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Indocin (Indomethacin)

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Indocin is an effective medication which helps to fight with pain or inflammation caused by many conditions such as gout, ankylosing spondylitis, arthritis, bursitis, or tendinitis. Indocin acts by reducing hormones that cause inflammation and pain in the body. It is nonsteroidal anti-inflammatory drug.

Other names for this medication:

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Also known as:  Indomethacin.


Indocin is a perfect remedy, which helps to fight against pain or inflammation caused by many conditions such as gout, ankylosing spondylitis, arthritis, bursitis, or tendinitis.

Indocin acts by reducing hormones that cause inflammation and pain in the body.

Indocin is also known as Indometacin, Indocid, Inmecin, Indochron E-R, Indocin-SR, Flexin Continus, Indolar, Indomax, Indomod, Pardelprin, Rheumacin, Rimacid, Slo-Indo.

It is nonsteroidal anti-inflammatory drug.


Shake the liquid form of Indocin before using.

Take Indocin tablets and liquid form orally with water.

Take Indocin once or twice a day at the same time.

Do not crush or chew it.

If you want to achieve most effective results do not stop taking Indocin suddenly.


If you overdose Indocin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Indocin overdosage: vomiting, migraine, lightheadedness, confusion, extreme tiredness, feeling of numbness, pricking, burning, creeping on the skin, convulsions, dyspepsia.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Indocin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Indocin if you are allergic to Indocin components.

Do not take Indocin if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Indocin if you are taking angiotensin ii receptor antagonists such as candesartan (atacand), eprosartan (teveten), irbesartan (avapro), losartan (cozaar), olmesartan (benicar), telmisartan (micardis), and valsartan (diovan); beta blockers such as atenolol (tenormin), labetalol (normodyne), metoprolol (lopressor, toprol xl), nadolol (corgard), and propranolol (inderal); cyclosporine (neoral, sandimmune); digoxin (lanoxin); diuretics ('water pills') such as triamterene (dyrenium, in dyazide); lithium (eskalith, lithobid); methotrexate (rheumatrex); phenytoin (dilantin); and probenecid (benemid), angiotensin-converting enzyme (ace) inhibitors such as benazepril (lotensin), captopril (capoten), enalapril (vasotec), fosinopril (monopril), lisinopril (prinivil, zestril), moexipril (univasc), perindopril (aceon), quinapril (accupril), ramipril (altace), and trandolapril (mavik).

It can be dangerous to use Indocin if you suffer from or have a history of seizures, parkinson's disease, depression or mental illness, or liver or kidney disease.

Be careful with Indocin if you are planning to use indomethacin suppositories.

Be careful with Indocin if you had proctitis (inflammation of the rectum) or have recently had rectal bleeding, asthma, frequent stuffed or runny nose or nasal polyps (swelling of the lining of the nose).

Avoid alcohol.

Be careful with Indocin if you are going to have a surgery.

Avoid driving machine.

Do not stop take it suddenly.

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EcN did not exert long-term liveability in the porcine intestine. All experimental pigs remained methanogenic. Indomethacin and EcN administered together might produce the worst impact on bacteriocinogeny.

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To investigate the effects of nilotinib in a rat model of indomethacin-induced enterocolitis.

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Pheochromocytomas are tumors that may produce a variety of substances in addition to catecholamines. To date, among several cases of systemic inflammatory syndrome associated with interleukin-6 (IL-6) secretion, IL-6-producing pheochromocytomas, have been reported. However, the mechanism underlying IL-6 oversecretion in these cases has not yet been clarified. This report describes a patient with pheochromocytoma who exhibited pyrexia and marked inflammatory signs including C-reactive protein elevation. The inflammatory symptoms were easily controlled by the administration of loxoprofen, a nonsteroidal anti-inflammatory drug. The plasma concentration of IL-6 and 11-d-TXB(2), a stable metabolite of thromboxane A(2) (TXA(2)), were significantly elevated in parallel with an elevation of norepinephrine in the samples obtained by selective venous sampling. A left adrenalectomy was performed, and the acute inflammatory symptoms naturally diminished without loxoprofen. Cultured tumor cells obtained from the resected specimen spontaneously released IL-6, and indomethacin inhibited the IL-6 release. According to a cDNA microarray analysis, mRNA of protein kinase C-delta (PKC-delta), prostaglandin D synthase, and arachidonate release-relating enzymes were significantly overexpressed in the tumor tissue in comparison to the adjacent nontumor tissue. The constitutive phosphorylation of PKC-delta was observed in the tumor tissue. These results strongly suggest that the systemic inflammatory syndrome in IL-6-producing pheochromocytoma, at least in part, is caused by the overexpression of PKC-delta, resulting in an excess of arachidonate derivatives such as prostaglandins.

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A patent ductus arteriosus (PDA) often complicates the clinical course of preterm infants and increases the risk of intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), chronic lung disease (CLD) and death. The standard treatment to close a PDA is indomethacin. Its use is associated with renal, gastrointestinal and cerebral side-effects. Ibuprofen has been shown to be effective in closing a PDA without reducing blood flow velocity to the brain, gut or kidneys.

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The rhizome of Atractylodes macrocephala (Compositae) is one of the most well-known traditional Chinese medicine in China, Japan and Korea, which has a long history of use for the treatment of splenic asthenia, edema, anorexia, and excessive perspiration, etc. As active compounds of anti-inflammatory activity of this medicinal plant have not been fully elucidated, the aim of this study was to isolate and identify the active constituents inhibiting nitric oxide (NO) production from the rhizomes of A. macrocephala.

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This study examined endothelium-derived mediators of acetylcholine-induced relaxation in male rat femoral arteries. Arterial rings were suspended in a myograph for the measurement of isometric force. The generation of hydrogen peroxide (H2O2) in endothelial cells was detected using the fluorescent probe, 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate acetyl ester. N(G)-nitro-L-arginine methyl ester (L-NAME, NOS inhibitor) and 1H-[1,2,4]oxadiazolo[4,2-alpha]quinoxalin-1-one (ODQ, guanylate cyclase inhibitor) alone or in combination with indomethacin (cycloxygenase inhibitor) diminished acetylcholine-induced endothelium-dependent relaxation to a similar extent. A small relaxation to acetylcholine in 60 mM KCl-constricted rings was abolished by L-NAME. Acetylcholine-induced relaxation was reduced by charybdotoxin plus apamin (intermediate- and small-conductance Ca2+-activated K+ channel blockers, respectively) or by 30 mM KCl. Both ouabain (Na+/K+ ATPase inhibitor) and BaCl2 (K(IR) channel blocker) also inhibited the relaxation albeit to a lesser degree. In the presence of L-NAME, ODQ plus indomethacin, charybdotoxin plus apamin or ouabain plus BaCl2 produced further inhibition. Catalase attenuated acetylcholine-induced relaxations and this attenuation was prevented by 3-amino-1,2,4-triazole (catalase inhibitor). Catalase did not affect acetylcholine-induced relaxations in rings treated with L-NAME or ODQ. Acetylcholine increased the dichlorofluorescein fluorescence intensity in native endothelial cells and this effect was abolished by catalase and by L-NAME. Exogenous H2O2 caused endothelium-independent relaxation that was slightly inhibited by iberiotoxin, ODQ or significantly reduced by elevated KCl, and abolished by catalase. The present results indicate that in addition to nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF, sensitive to charybdotoxin plus apamin, ouabain, and BaCl2), the endothelium of rat femoral artery can release H2O2 in response to acetylcholine, which was sensitive to L-NAME. Thus, the eNOS-dependent H2O2 is likely to be the third mediator of acetylcholine-mediated relaxations in rat femoral arteries.

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Successful treatment at 60 minutes occurred in 35 of 40 (87.5%) of Spasmofen-treated patients and in 33 of 40 (82.5%) of ketorolac-treated patients. The difference was not statistically significant by Fisher's exact test (P=0.755). The mean percentage reduction of VPAS after 15 minutes was 61.82% in the Spasmofen-treated group and 64.76% in the ketorolac-treated group. The difference was also not statistically significant by the Z-test for proportions (P=0.795). Sixty minutes after being treated, Spasmofen was associated with a statistically significant greater reduction in VPAS (mean% reduction =92.36%) than ketorolac (75.06%; P=0.0466).

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For the treatment of post-traumatic stiff elbow, with careful open arthrolysis and early active and active-assisted exercise we can get good results.

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The preoperative administration of nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to have a positive impact on postoperative pain, but there is little research regarding the use of rectal NSAIDs given before surgery. The purpose of this study was to evaluate the effects of rectally administered indomethacin on postoperative pain in patients undergoing open cholecystectomy. A randomized controlled design was used to compare rectally administered indomethacin with placebo. Pain intensity, total opioid dose, and postoperative time to first request for analgesic were evaluated. The indomethacin group experienced significantly less postoperative pain and required less total opioid dose compared with the placebo group. Preoperative rectal administration of indomethacin reduces postoperative pain in open cholecystectomy when compared with placebo.

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Ketorolac inhibition of ureteral contractility was dose dependent. At 90 minutes, the average percent decrease from the spontaneous contraction rate for 0.1 nM ketorolac was 18.2%; 1 nM, 34.3%; 10 nM, 56.0%; 100 nM, 69.9%; 1 microM, 88.7%; and 10 microM, 98.3%. Ureteral contractility was significantly reduced by 1 microM ketorolac (39.0%; P = 0.016) at 15 minutes when compared with DMSO. In addition, 1 microM ketorolac was not significantly different at any time point from any of the higher doses studied.

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Patients scheduled to undergo phacoemulsification and with no recognized CME risks (diabetic retinopathy, retinal vascular disease, or macular abnormality) were randomized to receive either prednisolone acetate 1% 4 times daily (QID) alone (steroid group; n = 278) or prednisolone 1% QID plus ketorolac 0.4% QID (ketorolac/steroid group; n = 268) for approximately four weeks postoperatively. In the ketorolac/steroid group, patients also received topical ketorolac 0.4% QID for three days preoperatively. In both groups, patients received four doses of ketorolac 0.4% one hour before surgery. Patients with capsular disruption or vitreous loss intraoperatively were exited from the study. Outcome measures included CME incidence, retinal thickness as measured by optical coherence tomography (OCT), best-corrected visual acuity, and contrast sensitivity.

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A total of 105 patients (26-64 years old) suffering from primary osteoarthritis (OA) of the knee were enrolled in this international, multicenter, randomized, double blind controlled trial. Fifty three patients were given ACE and 52 CEL. They were treated with either 90 mg bid of slow release ACE or 200 mg bid of CEL for 6 weeks. Additional gastroprotective therapy was not provided. Tolerability was assessed by physical examination, laboratory tests, vital signs and reports of side effects, as well as by patient and physician global assessments. Efficacy parameters comprised pain assessment by visual analogue scale (VAS) and ordinal scale, WOMAC, SF-36 and patient and physician global impressions of efficacy. In addition, acetaminophen consumption was recorded.

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Resveratrol showed biphasic activity in indomethacin-induced gastric ulcerated mice. A protective effect at a lower dose (2 mg kg(-1)) and a contraindicative effect at a higher dose of Resveratrol (10 mg kg(-1)) were observed. This phenomenon was possibly controlled by a COX-1 and eNOS balance, which ultimately maintained angiogenesis in Resveratrol-treated pre-ulcerated mice. The lower dose of Resveratrol (2 mg kg(-1)) augmented eNOS expression without altering COX-1 expression, but, at a higher dose (10 mg kg(-1)), Resveratrol predominantly suppressed COX-1 expression, which significantly reduced both PGE2 synthesis and angiogenesis. Thus it ultimately resulted in delay healing of indomethacin-induced gastric ulcers. Hence, it could be concluded that COX-1 and eNOS acted as key regulatory factors switching the biphasic effects of Resveratrol in indomethacin-induced ulcerated mice.

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Eupatorium aschenbornianum is considered useful in the treatment of gastric ulcer. In the current study the validity of this practice was tested by using the experimental model of an ethanol induced gastric ulcer in rats. The results show that E. aschenbornianum had gastroprotective activity, that the hexane extract had the highest protective activity (85.65+/-4.76%), and that encecanescin isolated from this extract was the main active gastroprotective agent. The effect elicited by encecanescin was attenuated by N(G)-nitro-L-arginine methyl ester, N-ethylmaleimide and indomethacin, which suggests that NO, prostaglandins and sulfydryl groups are involved in the mechanisms of gastroprotective action.

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To assess the clinical benefit, relative efficacy, and pharmacokinetic-response curve of preoperative and postoperative ketorolac tromethamine 0.4% (Acular LS) to improve outcomes during and after cataract surgery.

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This study evaluated the inhibitory action of luteolin-7-O-beta-D-glucuronopyranoside, luteolin which was isolated from Salix gilgiana leaves, and omeprazole on reflux esophagitis and gastritis in rats. Reflux esophagitis and gastritis were induced surgically and by the administration of indomethacin, respectively. The intraduodenal administration of luteolin-7-O-beta-D-glucuronopyranoside decreased the ulcer index, injury area, gastric volume and acid output, and increased the gastric pH compared with luteolin. Luteolin-7-O-beta-D-glucuronopyranoside significantly decreased the size of the gastric lesions that had been induced by exposing the gastric mucosa to indomethacin. The malondialdehyde content, which is the end product of lipid peroxidation, was increased significantly after inducing of reflux esophagitis. The malondialdehyde content was decreased by Luteolin-7-O-beta-D-glucuronopyranoside but not luteolin or omeprazole. Luteolin-7-O-beta-D-glucuronopyranoside has a more potent antioxidative effect than luteolin. Luteolin-7-O-beta-D-glucuronopyranoside is a promising drug for the treatment of reflux esophagitis and gastritis.

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The protein synthesis inhibitor dexamethasone (1 micromol/l), the non-selective cyclooxygenase inhibitor indomethacin (10 micromol/l), the selective cyclooxygenase-2 inhibitor NS 398 (1 micromol/l), and the thromboxane A2/prostaglandin H2 (TP) receptor antagonist SQ 29,548 (1 micromol/l), reduced the concentration-response curves to phenylephrine more in segments from hypertensive than from normotensive rats; however, the thromboxane A2 (TxA2) synthase inhibitors furegrelate (10 micromol/l) and OKY 046 (1 and 10 micromol/l) had no effect in either strain. Removing endothelium or adding dexamethasone almost abolished the NS 398 effect. Cyclooxygenase-2 protein expression, which was reduced by dexamethasone, was higher in aorta from hypertensive animals. In both strains cyclooxygenase-2 was localized mainly in endothelial cells and adventitial fibroblasts. 13,14-Dihydro-15-keto-PGF2alpha, 6-keto-PGF1alpha and 8-isoprostane levels were greater in the medium from hypertensive than from normotensive rats; NS 398 decreased levels of the three metabolites studied only in the medium from SHR.

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Proteinase-activated receptor (PAR)-1 or -2 modulates gastrointestinal transit in vivo. To clarify the underlying mechanisms, we characterized contraction/relaxation caused by TFLLR-NH2 and SLIGRL-NH2, PAR-1- and -2-activating peptides, respectively, in gastric and small intestinal (duodenal, jejunal and ileal) smooth muscle isolated from wild-type and PAR-2-knockout mice. Either SLIGRL-NH2 or TFLLR-NH2 caused both relaxation and contraction in the gastrointestinal preparations from wild-type animals. Apamin, a K+ channel inhibitor, tended to enhance the peptide-evoked contraction in some of the gastrointestinal preparations, whereas it inhibited relaxation responses to either peptide completely in the stomach, but only partially in the small intestine. Indomethacin reduced the contraction caused by SLIGRL-NH2 or TFLLR-NH2 in both gastric and ileal preparations, but unaffected apamin-insensitive relaxant effect of either peptide in ileal preparations. Repeated treatment with capsaicin suppressed the contractile effect of either peptide in the stomach, but not clearly in the ileum, whereas it enhanced the apamin-insensitive relaxant effect in ileal preparations. In any gastrointestinal preparations from PAR-2-knockout mice, SLIGRL-NH2 produced no responses. Thus, the inhibitory component in tension modulation by PAR-1 and -2 involves both apamin-sensitive and -insensitive mechanisms in the small intestine, but is predominantly attributable to the former mechanism in the stomach. The excitatory component in the PAR-1 and -2 modulation may be mediated, in part, by activation of capsaicin-sensitive sensory nerves and/or endogenous prostaglandin formation. Our study thus clarifies the multiple mechanisms for gastrointestinal motility modulation by PAR-1 and -2, and also provides ultimate evidence for involvement of PAR-2.

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We used the partial protection exerted by suitable dosages of nicotinamide against the beta-cytotoxic effect of streptozotocin (STZ) to create an experimental diabetic syndrome in adult rats that appears closer to type II diabetes mellitus than other available animal models. The dosage of 230 mg/kg of nicotinamide given intraperitoneally 15 min before STZ administration (65 mg/kg i.v.) yielded animals with hyperglycemia (187.8 +/- 17.8 vs. 103.8 +/- 2.8 mg/dL in controls; P < 0.001) and preservation of plasma insulin levels. This study assessed the relationship between endothelial dysfunction and agonist-induced contractile responses in such rats. In the thoracic aorta, the acetylcholine (ACh) induced relaxation was significantly reduced and the noradrenaline (NA) induced contractile response was significantly increased in diabetic rats compared with age-matched control rats. In the superior mesenteric artery, the ACh-induced relaxation was similar in magnitude between diabetic and age-matched control rats; however, the ACh-induced endothelium-derived hyperpolarizing factor (EDHF) type relaxation was significantly weaker in diabetic rats than in the controls. The phenylephrine (PE) induced contractile response was not different between the two groups. The plasma concentration of NOx (NO2- + NO3-) was significantly lower in diabetic rats than in control rats. We conclude that vasomotor activities in conduit arteries are impaired in this type II diabetes model.

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Haemodynamic instability affects 22% to 29% of very low birth weight infants in the acute period following ligation of the ductus arteriosus and contributes to the mortality seen in this group. Since the sudden elevation of systemic vascular resistance has been recognised to be one of the factors contributing to this instability, milrinone, an afterload reducing agent, might potentially be of significant therapeutic benefit. This report presents the clinical course of an infant born at 26 weeks gestation who required surgical ligation of a haemodynamically significant patent ductus arteriosus after two unsuccessful 6-day courses of intravenous indomethacin. The post-operative period was characterized by oxygenation failure, rising blood pressure and echocardiographic signs indicative of diastolic dysfunction. The infant was successfully managed with milrinone, a phosphodiesterase inhibitor, which acts both as an "inodilator" and has lusitropy properties. Post-duct ligation haemodynamic instability in a preterm infant was successfully managed with milrinone. The role of afterload-reducing agents such as milrinone in this setting should, therefore, be systematically analyzed.

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We previously reported that eupatilin (5,7-dihydroxy-3,4,6-trimethoxyflavone) extracted from Artemisia asiaitica, augmented the cellular antioxidant defense capacity through induction of the antioxidant protein heme oxygenase-1 (HO-1), thereby protecting ileal smooth muscle cells from nonsteroidal anti-inflammatory drug (NSAID)-induced intestinal toxicity. In the present study, we used cultured feline esophageal epithelial cells (EEC) to investigate the ability of eupatilin to induce expression of HO-1 and to analyze its cytoprotective effect against indomethacin-induced damage, since NSAID users have a higher risk of esophageal ulcers or esophagitis than non-NSAID users. A culture of EEC from cat was prepared. The identity of the cultures was confirmed by immunocytochemistry using cytokeratin antibodies. Western blot analysis showed a concentration- and time- dependent expression of HO-1 in response to eupatilin. Phosphorylation of extracellular regulating protein kinase (ERKs) and Akt, and nuclear translocation of nuclear related factor 2 (Nrf2) were induced by 150 microM eupatilin in a time-dependent manner. Eupatilin-induced HO-1 expression and Nrf2 were partly attenuated by MEK inhibitor PD98059 and almost completely by phosphatidyl-inactiol 3 kinase (PI3K) inhibitor LY294002, but not by c-Jun N-terminal kinase (JNK) inhibitor SP600125 or p38 mitogen activated protein kinase (MAPK) inhibitor SB202190. MTT assay showed that treatment with 2 mM indomethacin for 2 h decreased cell viability to about 41%. Pre-treatment of cells with eupatilin resulted in the dose-dependent inhibition of indomethacin-induced cell damage. We confirmed that ZnPP, an HO-1 inhibitor, repressed eupatilin-induced HO-1 activity and showed the protective effect of eupatilin against indomethacin-induced cell injury. The data suggested that HO-1 was partly responsible for the eupatilin-mediated protective action of esophageal epithelial cells against indomethacin via both ERKs and PI3K/Akt pathways as well as Nrf2 translocation.

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We investigated the effect of levosimendan on contractile tone of human isolated internal mammary artery (IMA). The responses in IMA were recorded isometrically by a force-displacement transducer in isolated organ baths. Levosimendan was added to organ baths either at rest or after precontraction with phenylephrine (1 micromol/L). Levosimendan-induced relaxations were tested in the presence of cyclooxygenase inhibitor indomethacin (10 micromol/L), nitric oxide synthase inhibitor N122-nitro-L-arginine methyl ester (100 micromol/L), large-conductance calcium-activated potassium-channel inhibitor tetraethylammonium (1 mmol/L), adenosine triphosphate-sensitive potassium-channel inhibitor glibenclamide (10 micromol/L), and voltage-sensitive potassium-channel inhibitor 4-aminopyridine (1 mmol/L).

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LGP enhances Cl(-) secretion that is mostly mediated through the release of cyclooxygenase metabolites, by which provided an osmotic force for the subsequent laxative action observed in the rat constipation model.

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Hypothalamic neuropeptides influence the main components of energy balance: metabolic rate, food intake, body weight as well as body temperature, by exerting either an overall anabolic or catabolic effect. The contribution of alarin, the most recently discovered member of the galanin peptide family to the regulation of energy metabolism has been suggested. Our aim was to analyze the complex thermoregulatory and food intake-related effects of alarin in rats. Adult male Wistar rats received different doses of alarin (0.3; 1; 3 and 15μg corresponding approximately to 0.1, 0.33, 1, and 5 nmol, respectively) intracerebroventricularly. Regarding thermoregulatory analysis, oxygen consumption (indicating metabolic rate), core temperature and heat loss (assessed by tail skin temperature) were recorded in an Oxymax indirect calorimeter system complemented with thermocouples and Benchtop thermometer. In order to investigate potential prostaglandin-mediated mechanisms of the hyperthermic effect of alarin, effects of intraperitoneally applied non-selective (indomethacin, 2mg/kg) or selective cyclooxygenase inhibitor (COX-2 inhibitor meloxicam, 1; 2mg/kg) were tested. Effects of alarin on daytime and nighttime spontaneous food intake, as well as, 24-h fasting-induced re-feeding were recorded in an automated FeedScale system. Alarin increased oxygen consumption with simultaneous suppression of heat loss leading to a slow coordinated rise in core temperature. Both applied COX-inhibitors suppressed this action. Alarin failed to induce daytime food intake, but suppressed spontaneous nighttime and also fasting-induced re-feeding food intake. Alarin appears to elicit a slow anorexigenic and prostaglandin-mediated, fever-like hyperthermic response in rats. Such a combination would characterize a catabolic mediator. The potential involvement of alarin in sickness behavior may be assumed.

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Nuclear inclusions formed by the aggregation of a polyalanine expansion mutant of the nuclear poly(A)-binding protein (PABPN1) is a hallmark of oculopharyngeal muscular dystrophy (OPMD). OPMD is a dominant autosomal disease in which patients exhibit progressive difficulty of swallowing and eyelid elevation, starting around the age of 50. At present, there is no specific treatment to reduce the aggregate burden in patients. However, in cell culture models of OPMD, reduction of protein aggregation can be achieved by ectopic expression of HSP70. As gene transfer may not be the most effective means to elevate HSP70 levels, we tested four pharmacological agents for their ability to induce HSP70, recruit both HSP70 and HSC70 into the cell nucleus and reduce mutant PABPN1 aggregation in a HeLa cell culture model. We show here that exposure to moderate levels of ZnSO4, 8-hydroxyquinoline, ibuprofen and indomethacin produced a robust stress response resulting in the induction of HSP70 in HeLa cells expressing the mutant PABPN1 as a green fluorescent protein (GFP) fusion protein. Both HSP70 and the constitutive chaperone HSC70 localized in the nucleus of cells treated with any one of the four agents. This stress response was similar to what was observed following hyperthermia. All four agents also caused a significant reduction in the cellular burden of protein aggregates, as was judged by confocal microscopy and solubility changes of the aggregates. A concomitant reduction of cell death in drug-treated mutant PABPN1 expressing cells was also observed.

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Disruption of the blood-brain barrier (BBB) occurs in many diseases and is often mediated by inflammatory and neuroimmune mechanisms. Inflammation is well established as a cause of BBB disruption, but many mechanistic questions remain.

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In the present study, we investigated the effect of ET-1 on diabetic glomeruli that were freshly isolated from Wistar rats after streptozotocin-induced diabetes for 1 week (DM1W), 1 month (DM1M) and 3 months (DM3M), respectively, and then observed the glomerular uptake of [(3)H]-labelled thymidine and the production of fibronectin.

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Under urethane anesthesia, a chambered stomach or a proximal duodenal loop was superfused with saline, and HCO3- secretion was measured at pH 7.0 using a pH-stat.

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In a prospective, randomized, double-blind, placebo-controlled study, patients intravenously received placebo, dexamethasone 4 mg, or dexamethasone 8 mg immediately before induction of anesthesia. A standard anesthetic technique, including sevoflurane and air in oxygen, was used. Postoperatively, emetic symptoms (nausea, retching, and vomiting) and analgesic requirement were evaluated by an investigator.

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Of the 11 species tested, 2 showed a vasorelaxant effect. Further investigation of the mechanisms of action of the aqueous extract of green alga, Cladophora patentiramea (AECP),showed that the vascular relaxant effect was endothelium- and concentration-dependent. A maximum relaxation of 45.8 +/- 4.6% (n = 8, p < 0.001) was obtained at 0.1 mg/ml of extract, after which the response was found to reduce in a concentration-dependent manner to 15.7 +/- 4.9% (n = 8, p < 0.001) at the highest extract concentration tested. Pretreatment of endothelium-intact aortic rings with Nomega-nitro-L-arginine methyl ester (L-NAME, 30 microM), (1)H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 microM) and methylene blue (100 microM) resulted in a complete blockade of AECP-induced vasorelaxation. However, the relaxant effects of the extract were not blocked by atropine (1 microM), indomethacin (10 microM) and glibenclamide (10 microM), although the maximum relaxant responses were enhanced in the presence of glibenclamide.

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12 of the 186 patients included discontinued their medication before the end of the trial due to side effects. The remaining 174 patients were included in the analysis. In the indomethacin group (n = 89), 77 patients (87%) showed no HO, 9 showed HO of grade 1 and 3 showed HO of grade 2 according to the Brooker classification. In the rofecoxib group (n = 85) 73 patients (86%) showed no ossification, 9 showed grade 1, and 3 showed grade 2.

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indocin 25mg capsules 2015-02-08

The present study provides direct evidence that exposure to LPS results in induction of iNOS and SOD associated with noradrenaline hyporeactivity, while increased NO is only measured when l-arginine is present. A catalase-sensitive buy indocin online mechanism and release of NO from N-acetylcysteine-sensitive stores could also contribute to the vascular hyporeactivity.

indocin online 2016-11-16

There were 25 infants treated with poractant alfa (27.1±1.6 weeks, birth weight 930±231 g) and 25 treated with beractant (26.7±1.7 weeks, P=0.407 and birth weight 898±282 g, P=0.666). Clinically significant PDAs were diagnosed and treated in 8 of 25 (32%) of the poractant alfa and 19 of 25 (76%) of the beractant group (P=0.002). Indomethacin treatment was slightly earlier (3.4±2.5 days) in the poractant alfa than in the beractant group (5.1±4.9 days, P=0.038). Right ventricle pressure (RVP)/systolic arterial pressure (SAP) ratio in the first week was slightly lower in the poractant alfa (64±20%) than in the beractant (78±26%, P=0.048) group. Following a second dose of surfactant, neither poractant alfa nor beractant changed PDA flow. These hemodynamic observations were associated buy indocin online with less respiratory support in the poractant alfa group, allowing earlier extubation (13 of 25 at 48 h and 15 of 25 at 72 h), than in the beractant group (6 of 25 at 48 h, P=0.044, and 8 of 25 at 72 h, P=0.049).

indocin renal dosing 2016-08-19

In the present study, we investigated the implication of transient receptor potential vanilloid (TRPV)-related channels in the 5-hydroxytryptamine (5-HT)-induced both intracellular calcium response and mitogenic effect in rat pulmonary arterial smooth muscle cells (PASMC). Using microspectrofluorimetry (indo-1 as Ca(2+) fluorescent probe) and the patch-clamp technique (in whole-cell configuration), we found that 5-HT (10 microM) induced a buy indocin online transient intracellular calcium mobilization followed by a sustained calcium entry. This latter was partly blocked by an inhibitor of cytochrome P450 epoxygenase (17-ODYA) and insensitive to cyclo-oxygenase and lipoxygenase inhibitors (indomethacin and CDC), suggesting the involvement of arachidonic acid metabolization by cytochrome P450 epoxygenase. This calcium influx was also sensitive to Ni(2+) and to ruthenium red, a TRPV channel blocker, and mimicked by 4alpha-phorbol-12,13-didecanoate (4alpha-PDD), a TRPV4 channel agonist. In patched PASMC, 5-HT and 4alpha-PDD-activated TRPV4-like ruthenium red sensitive currents with typical characteristics. Furthermore, 5-HT induced a ruthenium red sensitive increase in BrdU incorporation levels in PASMC. The present study provides evidence that 5-HT activates a TRPV4-like current, potentially involved in PASMC proliferation. The signalling pathway between proliferation and ion channel activation remains to be determined and may represent a molecular target for the treatment of vascular diseases such as pulmonary hypertension.

indocin gout dose 2017-03-10

The mean diclofenac concentration in the buy indocin online subretinal fluid was 42.31 (SD 24.89) ng/µL. Ketorolac was undetectable in the subretinal fluid in all patients who received it because ketorolac tromethamine levels were under the limit of detection. In the aqueous humour, mean diclofenac concentration was 4.98 (SD 4.56) ng/µL, and mean ketorolac concentration was 20.17 (SD 12.21) ng/µL. Topical administration of diclofenac sodium yielded 8.4 times greater drug concentration in the subretinal fluid than in the aqueous humour. Aqueous humour concentrations of ketorolac were higher than those of diclofenac (p = 0.019).

indocin generic 2017-03-22

Groups either received synbiotic (1.5 × 1010 CFU Ecologic® 825 + 10 g fructo-oligosaccharides (FOS P6) per day buy indocin online ) or control supplements for two weeks.

indocin dosage forms 2017-11-25

The protective effects of NSAIDs/ASA against oxidative damage are confined to a relatively buy indocin online small therapeutic window.

indocin user reviews 2015-10-16

A novel microwave electrode with a cooled tip (FORSEA MTC-3 type, China) was devised to better enable microwave ablation of liver cancers. The efficacy of this technology was evaluated. The records of 160 patients (97 with hepatoma, 63 with metastatic cancer of the liver) who had undergone microwave ablation with this new device were reviewed. One-year survival in 86 patients whose follow-up had been more than one year was determined. Pre-operative and post-operative contrast-enhanced CT scans were performed to assess completion of therapy and the presence or absence of recurrent tumor. For patients with hepatoma, serum alpha-fetoprotein (AFP) levels were evaluated pre-operatively and, if elevated, post-operatively. A median two (range one to five) applications were required per session. All patients exhibited initial radiographic resolution of their lesions after therapy. The ablated areas were not enhanced in any phases of contrast CT scan. Eight patients required a second microwave therapy for recurrent tumor; two patients required a third treatment. Twenty-five patients with hepatoma had elevated AFP (104.2+/-22.5 ng/ml), which, after microwave ablation, recovered to normal or almost normal (24.6+/-3.6 ng/ml) (t = 2.1, p<0.05). There were no post-operative deaths. Complications included fever in three of four patients, successfully treated with indomethacin, elevated transaminases in four of five patients, requiring no treatment except for those with pre- buy indocin online operative ascites (who were dialyzed), pleural effusions in fourteen patients, only one of whom required drainage, and obstructive jaundice requiring drainage in two patients. The one-year survival rate was 91.9%. Microwave ablation with this novel cooled-tip electrode is safe, minimally invasive and effective. The tool may greatly expand the fraction of patients with liver cancer who might be candidates for microwave ablation.

indocin brand name 2016-09-11

Glycosmis pentaphylla, Tridax procumbens, and Mangifera indica are well-known plants available throughout India and they are commonly used for the treatment of various diseases including buy indocin online arthritis. The polyherbal formulation was formulated using the ethanol extracts of the stem bark of G. pentaphylla , whole plant of T. procumbens, and leaves of M. indica. The polyherbal formulation contains the ethanol extracts of G. pentaphylla, T. procumbens, and M. indica in the ratio of 2:2:1. The quality of the finished product was evaluated as per the World Health Organization's guidelines for the quality control of herbal materials. Arthritis was induced in female Wistar rats using Freund's complete adjuvant (FCA), and the antiarthritic effect of polyherbal formulation was studied at doses of 250 and 500 mg/kg. The effects were compared with those of indomethacin (10 mg/kg). At the end of the study, blood samples were collected for biochemical and hematological analysis. The radiological examination was carried out before terminating the study.

indocin tablets 2015-04-09

The diabetic state significantly increased the maximum contractile response to buy indocin online KCl and NA (P < 0.01-0.005) and reduced the maximum relaxation due to ACh (P < 0.01) as compared to controls and treatment with TFG extract in the diabetic group significantly improved these changes relative to the untreated diabetic group (P < 0.05). With L-NAME pretreatment, no significant difference between diabetic and extract-treated diabetic groups was found out. On the other hand, there was a significant difference between these two groups following INDO pretreatment (P < 0.05).

indocin 50mg capsules 2015-10-09

Eligible infants born <29 weeks buy indocin online were screened for a large PDA and received indomethacin or placebo before age 12 h.

indocin pain medication 2016-06-22

Nonsteroidal anti-inflammatory drugs (NSAID) have shown chemopreventive effects in both preclinical and clinical studies; however, the precise molecular mechanism governing this response remains unclear. We used DNA microarray techniques to search for genes whose expression is induced by the NSAID indomethacin in human gastric carcinoma (AGS) cells. Among identified genes, we focused on those related to tight junction function (claudin-4, claudin-1, and occludin), particularly claudin-4. Induction of claudin-4 by indomethacin was confirmed at both mRNA and protein levels. NSAIDs, other than indomethacin (diclofenac and celecoxib), also induced claudin-4. All of the tested NSAIDs increased the intracellular Ca2+ concentration. Other drugs that increased the intracellular Ca2+ concentration (thapsigargin and ionomycin) also induced claudin-4. Furthermore, an intracellular Ca2+ chelator [1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid] inhibited the indomethacin-dependent induction of claudin-4. These results strongly suggest that induction of claudin-4 by indomethacin is mediated through an increase in the intracellular Ca2+ concentration. Overexpression of claudin-4 in AGS cells did not affect cell growth or the induction of apoptosis by indomethacin. On the other hand, addition of indomethacin or overexpression of claudin-4 inhibited cell migration. Colony formation in soft agar was also inhibited. Suppression of claudin-4 expression by small interfering RNA restored the migration activity of AGS cells in the presence of indomethacin. Based on these results, we consider that the induction of claudin-4 and other tight junction-related genes by NSAIDs may be involved in the chemopreventive effect of buy indocin online NSAIDs through the suppression of anchorage-independent growth and cell migration.

indocin drug 2017-11-09

We included four RCTs, involving 564 participants in this review. We compared the effects of colchicine in addition to a non-steroidal anti-inflammatory drug (NSAID) such as ibuprofen, aspirin or indomethacin to the effects of the NSAID alone. Two comparable trials studied the effects of colchicine in 204 participants with buy indocin online recurrent pericarditis and two trials studied 360 people with acute pericarditis. All trials had a moderate quality for the primary outcomes. We identified two on-going trials; one of these trials examines acute pericarditis and the other assesses recurrent pericarditis.There was moderate quality evidence that colchicine reduces episodes of pericarditis in people with recurrent pericarditis over 18 months follow-up (HR 0.37; 95% confidence interval (CI) 0.24 to 0.58). It is expected that at 18 months, the number needed to treat (NNT) is 4. In people with acute pericarditis, there was moderate quality evidence that colchicine reduces recurrence (HR 0.40; 95% CI 0.27 to 0.61) at 18 months follow-up. Colchicine led to a greater chance of symptom relief at 72 hours (risk ratio (RR) 1.4; 95% CI 1.26 to 1.56; low quality evidence). Adverse effects were mainly gastrointestinal and included abdominal pain and diarrhoea. The pooled RR for adverse events was 1.26 (95% CI 0.75 to 2.12). While the number of people experiencing adverse effects was higher in the colchicine than the control groups (9% versus 7%), the quality of evidence was low owing to imprecision, and there was no statistically significant difference between the treatment groups (P = 0.42). There was moderate quality evidence that treatment with colchicine led to more people stopping treatment due to adverse events (RR 1.87; 95% CI 1.02 to 3.41).

indocin gout dosage 2017-10-15

A pH- and enzyme-dependent colon-targeted multi-unit delivery system of indomethacin was developed by coating guar gum and Eudragit FS30D sequentially onto drug-loaded pellets in a fluidized bed coater. In vitro studies showed that smaller coating weight gain of guar gum resulted in reduced release lag time t10 (10% release time), but favored degradation by enzymes (galactomannanase). A cumulative weight gain (CWG) of 44% provided sufficient enzymatic sensitivity and protection of the core. Under gradient pH conditions (pH = 1.2, 6.8, 7.4 and 6.5 for 2, 2, 1 and 15 h, respectively), indomethacin was released from Eudragit FS30D-coated pellets quickly after changing pH to 7.4. For guar gum/Eudragit FS30D double-coated pellets, only about 5% of the drug was released after another 1 h, showing retarding effect by guar gum coating. After changing pH to 6.5 and addition of galactomannanase, enzyme-dependent drug release was observed. Pharmacokinetic study in beagle dogs showed that fastest absorption with the smallest Tmax and Tlag was buy indocin online observed for uncoated pellets. The Tmax and Tlag of Eudragit FS30D-coated pellets were postponed to about 2.5 and 1 h, respectively. After a further guar gum coating, Tlag was further postponed to about 2.8 h, about 2 h of additional lag time on the basis of Eudragit FS30D coating. It is indicated that the guar gum/Eudragit FS30D-coated system has potential to be used to deliver drugs to the colon.

indocin 50mg medication 2015-09-25

Primary stabbing headache is characterized by transient, cephalic ultrashort stabs of pain. It is a frequent complaint with a prevalence of 35.2%, a female preponderance, and a mean age of onset of 28 years (Vågå study). Attacks are generally characterized by moderate to severe, jabbing or stabbing pain, lasting from a fraction of a second to 3s. Attack frequency is generally low, with one or a few attacks per day. The paroxysms generally occur spontaneously, during daytime. Most patients exhibit a sporadic pattern, with an erratic, unpredictable alternation between symptomatic and non-symptomatic periods. Paroxysms are almost invariably unilateral. Temporal and fronto-ocular areas are most frequently affected. Attacks tend to move from one area to another, in either the same or the opposite hemicranium. Jabs may be accompanied by a shock-like feeling and even by head movement - "jolts" -or vocalization. On rare occasions, conjunctival hemorrhage and monocular vision loss have been described as associated features. Primary stabbing headache may concur, synchronously or independently, with other primary headaches. In contrast to what is the case in adults, in childhood it is not usually associated with other headaches. Treatment is rarely necessary. Indomethacin, 75-150 mg daily, may seem to buy indocin online be of some avail. Celecoxib, nifedipine, melatonin, and gabapentin have been reported to be effective in isolated cases and small series of patients. The drug studies need corroboration.

indocin suppository dosage 2017-10-04

The present study was undertaken in order to examine transduction mechanism involved in the single application of 100 μM homocysteine (Hcy) on isolated rat femoral artery Diovan Hct Reviews (RFA) rings equilibrated on the basal tone; to establish if a single application of 100 μM Hcy alters contractile effect of phenylephrine (Phe), or oppositely the relaxant effect of acetylcholine (ACh) or bradykinin (BK) after 60-min-long incubation of 100 μM Hcy; and finally to identify morphological changes on the vascular wall after a 24-h-long incubation of 100 μM Hcy. Hcy produced contractile response of intact RFA, which was increased after endothelial denudation, while decreased by urapidil (an α1 receptor blocker), nifedipine (a voltage-gated L-type Ca++ channel blocker) or indomethacin (a cyclooxygenase inhibitor). The initial RFA contraction evoked by Phe was further increased by the single addition of Hcy, which was not the case when ouabain (an inhibitor of Na+/K+-ATPase) was preincubated. After 60-min-long incubation of Hcy relaxant actions of ACh and BK were unaltered, equieffective and equipotent. A 24-h-long incubation of RFA rings with Hcy produced an impairment of vascular endothelium, expressed as a minor or more pronounced interruption of endothelial cells.

indocin gout medication 2015-01-23

Adjuvant induced arthritis is a chronic crippling, skeleton-muscular disorder having nearest approximation to human rheumatoid arthritis for which there is currently no medicine available effecting a permanent cure. Even modern drugs used for the amelioration of the symptoms, offer only temporary relief and also produce severe side effects. In the indigenous system of medicine, wood of Premna serratifolia Linn., is reported to be useful in the treatment of arthritis. It is a large shrub, distributed throughout Asia, used against a wide variety of diseases. However, no systematic study has been reported regarding its anti-arthritic activity. This work was aimed at the scientific validation of the ethno-pharmacological claim about its anti-arthritic property. In the present study, anti-arthritic activity of ethanol extract of Premna serratifolia Linn., wood is done by Freund's adjuvant induced arthritis model. Loss in body weight during arthritis condition was corrected on treatment with ethanol extract and standard drug, indomethacin. Biochemical parameters such as hemoglobin content, total WBC, RBC, erythrocyte and sedimentation rate were also estimated. The ethanol extract at the dose of 300 mg/kg body weight inhibited Amalaki Online the rat paw edema by 68.32% which is comparable with standard drug indomethacin 74.87% inhibition of rat paw edema after 21 days. The results of the current investigation concluded, ethanol extract of Premna serratifolia Linn., wood possess a significant anti-arthritic activity against adjuvant induced arthritis and justifying its therapeutic role in arthritic condition. The observed anti-arthritic activity may be due to the presence of phytoconstituents such as irridiod glycosides, alkaloids, phenolic compounds and flavonoids.

indocin oral suspension 2016-05-13

The aim of the work reported herein was to implement process analytical technology (PAT) tools during hot melt extrusion (HME) in order to obtain a better understanding of the relationship between HME processing parameters and the extruded formulations. For the first time two in-line NIR probes (transmission and reflectance) have been coupled with HME to monitor the extrusion of the water insoluble drug indomethacin (IND) in the presence of Soluplus (SOL) or Kollidon VA64 hydrophilic polymers. In-line extrusion monitoring of sheets, produced via a specially designed die, was conducted at various drug/polymer ratios and processing parameters. Characterisation of the extruded transparent sheets was also undertaken by using DSC, XRPD and Raman mapping. Analysis of the experimental findings revealed the production of molecular solutions where IND is homogeneously blended (ascertained by Raman mapping) in the polymer matrices, as it acts as a plasticizer for both hydrophilic polymers. PCA analysis of the recorded NIR signals showed that the screw speed used in HME affects the recorded spectra but not the homogeneity of the embedded drug in the polymer sheets. The IND/VA64 and IND/ Diamox 250 Dosage SOL extruded sheets displayed rapid dissolution rates with 80% and 30% of the IND being released, respectively within the first 20min.

indocin medication generic 2015-05-30

With improving neonatal survival for extremely premature babies, the challenge Symmetrel Brand Name for neonatology is to improve outcome of surviving babies. This review concentrates on best evidence emerging in recent years on prevention of brain damage by early administration of drugs as well as avoidance of induced brain damage by hyperventilation and dexamethasone therapy given postnatally for chronic lung disease.

indocin gel 2016-04-26

CCRE produced significant antiulcer activity against absolute ethanol, acidified ethanol and indomethacin induced gastric lesions. The pretreatment with L-NAME (10 mg/kg, p.o.), an inhibitor of nitric oxide synthesis and indomethacin (10 mg Mestinon 20 Mg /kg, s.c.), an inhibitor of prostaglandin production, reversed the antiulcer action of CCRE.

dosage of indocin 2017-04-30

To investigate the structural effect of polymeric excipients on the behavior of free volume of drug-polymer dispersions in relation Lasix Fluid Pill to glass transition.

indocin tab 2016-10-08

This retrospective pre/post comparative study was conducted in 3 tertiary hospitals that implemented CPOE in 2010. Two patient groups were compared: prior to (pre-CPOE) Elavil Max Dose and after (post-CPOE) CPOE implementation. Each group consisted of 230 randomly selected, high-acuity patients presenting to the ED with renal colic. The primary outcome was the proportion of patients receiving ketorolac in the ED. Secondary outcomes included choice of analgesic and average morphine dose.

indocin buy online 2017-07-11

Endothelium-dependent relaxations in human adult mesenteric microvessels involve 3 different Zovirax Pills Review main mechanisms: cyclooxygenase (COX)-derived prostanoids, nitric oxide (NO), and endothelium-derived hyperpolarizing factor (EDHF), which elicits vascular smooth muscle hyperpolarization and relaxation. There are some pathological conditions with an abnormal balance between mesenteric vasoconstriction and vasodilatation inputs leading to endothelial dysfunction and tissue injury.

indocin tablets uses 2016-06-01

Indomethacin treatment inhibited IgG1 and IgG2 production, and PGE2 restored both immunoglobulins in PWM-stimulated cultures. Remarkably, addition of IFN-gamma also restored IND-suppressed IgG2 but not IgG1. In contrast, addition of rIL (interleukin)-1alpha, rIL-1beta, rIL-6, or rIL-12 did not restore IgG2 responses. Furthermore, IND suppressed IFN-gamma production and PGE2 increased IFN-gamma levels. Kinetic studies indicate that PGE2 production occurred on the first day of culture, followed by IFN-gamma two days later.

indocin dosage chart 2016-06-11

Hyperthyroidism was induced by subcutaneous injections of L-thyroxine (T4) (0.5 mg/kg/day) for 3 days in order to investigate the effects of acute hyperthyroidism on the vasorelaxing responses to isoprenaline and acetylcholine in isolated rat aortae. In the aortae, there was no significant difference in isoprenaline-induced relaxation between hyperthyroid and control rats, however acetylcholine-induced relaxation was significantly greater in hyperthyroid rats than in control rats. N(G)-nitro-L-arginine (L-NOARG), an inhibitor of nitric oxide (NO) synthase, reduced isoprenaline- and acetylcholine-induced relaxations in both hyperthyroid and control rats and in the presence of L-NOARG no significant difference in the acetylcholine-induced relaxation was seen between the two groups of rats. Indomethacin, a cyclo-oxygenase inhibitor, had no significant influence on both isoprenaline- and acetylcholine-induced relaxations in both control and hyperthyroid rats. 17-Octadecynoic acid (17-ODYA), a cytochrome P-450 mono-oxygenase inhibitor, reduced the both isoprenaline- and acetylcholine-induced relaxation in both hyperthyroid and control rats, and acetylcholine-induced relaxation was still greater in hyperthyroid rats than in control rats. These results indicate that an acute hyperthyroidism significantly enhances muscarinic receptor- but not adrenoceptor-mediated relaxations of the aortae and L-NOARG abolished an enhancement by acute hyperthyroidism of muscarinic receptor-mediated relaxation, suggesting that the effects may be due to an alteration in muscarinic receptor-mediated NO systems of the aortae at early stage of hyperthyroidism.

indocin medication dosage 2015-12-14

In this prospective study, we compared the efficacy and side effects of indomethacin, ibuprofen, and paracetamol in patent ductus arteriosus (PDA) closure in preterm neonates. Three hundred preterm neonates with hemodynamically significant PDA (hs-PDA) admitted at our neonatal intensive care unit were enrolled in the study. They were randomized into three groups. Group I (paracetamol group) received 15 mg/kg/6 h IV paracetamol infusion for 3 days. Group II (ibuprofen group) received 10 mg/kg IV ibuprofen infusion followed by 5 mg/kg/day for 2 days. Group III (indomethacin group) received 0.2 mg/kg/12 h indomethacin IV infusion for three doses. Laboratory investigations such as renal function test, liver function test, complete blood count, and blood gases were conducted in addition to echocardiographic examinations. All investigations were done before and 3 days after treatment. There was no significant difference between all groups regarding efficacy of PDA closure (P = 0.868). There was a significant increase in serum creatinine levels and serum blood urea nitrogen (BUN) in the ibuprofen and indomethacin groups (P < 0.001). There was a significant reduction in platelet count and urine output (UOP) in both ibuprofen and indomethacin groups (P < 0.001). There was a significant increase in bilirubin levels in only the ibuprofen group (P = 0.003). No significant difference of hemoglobin (HB) level or liver enzymes in all groups (P > 0.05). Ventilatory settings improved significantly in patients with successful closure of PDA than those with failed PDA closure (P < 0.001).

indocin mg 2016-10-31

1. In the present study, we evaluated the role of cyclo-oxygenase (COX)-1 and COX-2 on gastric acid secretion in rabbit isolated parietal cells and gastric glands by examining [(14)C]-aminopyrine uptake, prostaglandin (PG) E(2) synthesis and COX-1, COX-2 and proton pump expression at baseline and after treatment with various concentrations of specific COX-1 (SC-560), COX-2 (5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methyl-sulphonyl)phenyl-2 (5H)-furanone; DFU) and non-specific COX (indomethacin) inhibitors. 2. In parietal cells, SC-560 and indomethacin, over the concentration range 10(-8) to 10(-4) mol/L, dose-dependently increased basal and 10(-4) mol/L histamine-stimulated aminopyrine uptake and inhibited PGE(2) synthesis, whereas DFU (10(-8) to 10(-5) mol/L) had no effect. However, at 10(-4) mol/L, DFU augmented histamine-stimulated aminopyrine uptake by 135% and inhibited PGE(2) synthesis by 39%, indicating an inhibition of COX-1 at this higher concentration. 3. The SC-560-, DFU- and indomethacin-induced augmentation of histamine-stimulated aminopyrine uptake was reduced to basal levels after 10(-5) mol/L lansoprazole treatment in parietal cells and gastric glands, whereas 10(-4) mol/L ranitidine only partially inhibited such augmentation. 4. Only COX-1 was detected in parietal cells. However, both COX-1 and COX-2 were expressed in gastric glands, with relative protein density of COX-1 being sixfold higher than that of COX-2. Protein levels of COX-1 in parietal cells and those of COX-1 and COX-2 in gastric glands remained unchanged, regardless of inhibitor treatment, either alone or with histamine. 5. Parietal cell proton pump expression was significantly enhanced by 10(-5) mol/L SC-560 and 10(-4) mol/L indomethacin (by 29 and 31%, respectively) and pump activity was enhanced by 61 and 65%, respectively. In contrast, 10(-5) mol/L DFU had no effect. 6. In conclusion, the data indicate that inhibition of COX-1- but not COX-2-derived PGE(2) synthesis is involved in augmentation of non-steroidal anti-inflammatory drug-induced gastric acid secretion in parietal cells by enhancing expression and activation of the proton pump.

indocin 25 mg 2017-02-06

Mercury chloride exposure for 30 days decreases NO bioavailability and increases oxidative stress. However, the mechanisms underlying the effects of mercury on the cardiovascular system are not completely understood, and it is not known if they are dose-dependent or if some concentrations have no harmful effects. Thus, we investigated the effects of chronic exposure to doses low (half) and high (2.5-fold higher) than that needed to obtain 29 nmol/L of HgCl2 on the vascular function. Three-month-old male Wistar rats received intramuscular (i.m.) HgCl2 for 30 days and were divided in three groups: lower (Low Hg); higher (High Hg); and saline was used as the control. High Hg exposure increased the contractile response to phenylephrine (PHE) in aortic rings, but Low Hg reduced it. The hyporesponsiveness in the Low Hg rats was blunted by endothelial denudation and NOS inhibition with l-NAME (100 μmol/L). The phosphorylated-eNOS/eNOS protein ratio increased in the aortas of Low Hg rats. In the High Hg group, endothelial denudation increased the PHE-induced contractions, while l-NAME had no effects and indomethacin (10 μmol/L), losartan (10 μmol/L) and apocynin (30 μmol/L) reduced this response. In the High Hg group, protein levels of the NADPH oxidase subunit gp91phox and cyclooxygenase-2 increased. Our results support previous suggestions that High Hg increases oxidative stress that might activate an inflammatory cascade and the renin-angiotensin system. However, very low Hg concentrations below the level considered safe still reduced vascular reactivity, suggesting the need for special attention to continuous exposure as a putative cause of increased cardiovascular risk.