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Modern combination therapy usually results in an 80-95% H. pylori eradication rate in compliant patients.
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of the 75 with severe stricture, 36 (48%) needed forcible dilatation only once, and 39 more often (13 twice, nine three times), most within 2 years. Only six of these patients need > or = 6 re-dilatations.
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Omeprazole blocks the action of H+,K+-ATPase in the gastric mucosa and thus inhibits the secretion of hydrochloric acid. We conducted a double-blind multicenter study (45 centers in 13 countries) of 602 patients with benign gastric or prepyloric ulcers to compare the effectiveness of omeprazole (20 mg once daily, 203 patients, or 40 mg once daily, 194 patients) and ranitidine, an H2-receptor antagonist (150 mg twice daily, 205 patients) in promoting ulcer healing and to evaluate the pattern of ulcer relapse during a six-month follow-up. Healing occurred at four weeks in 80 percent of the patients receiving 40 mg of omeprazole, 69 percent of those receiving 20 mg of omeprazole, 69 percent of those receiving ranitidine. At eight weeks, the corresponding figures were 96, 89, and 85 percent. A multivariate analysis of ulcer healing showed that at four weeks the ulcers of significantly more patients receiving omeprazole had healed as compared with patients receiving ranitidine (omeprazole, 40 mg, vs. ranitidine, P less than 0.0005; omeprazole, 20 mg, vs. ranitidine, P = 0.01). At eight weeks, the 40-mg dose of omeprazole was significantly more effective than ranitidine (P = 0.001) or the 20-mg dose of omeprazole (P = 0.03). Ulcer symptoms were relieved faster with omeprazole. In 68 patients receiving concurrent nonsteroidal antiinflammatory drugs, the healing rates at four weeks were 81 percent in the group receiving 40 mg of omeprazole, 61 percent in the group receiving 20 mg, and 32 percent in the group receiving ranitidine; at eight weeks, the corresponding figures were 95, 82, and 53 percent. During the six-month follow-up period (without treatment), significantly more patients in the omeprazole groups were free of symptoms and ulcers than in the ranitidine group. We conclude that in the dose used, omeprazole is superior to ranitidine in the treatment of benign gastric ulcers.
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Serum concentrations following administration of ranitidine and cimetidine were well described by the model, and parameter estimates obtained were in agreement with literature values. Simulations demonstrate the effects of various absorption parameters and gastroin-testinal tract transit parameters on bioavailability and plasma concentration profiles.
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The most common interactions concern cardiovascular drugs. The combination of calcium antagonists (CA) and beta-blockers is more effective than single-agent therapy in stable effort angina and hypertension. But there is an increased risk of hemodynamic or electrophysiological side effects in patients with left ventricular or sinus dysfunction, or disturbances of conduction. Pharmacokinetic interactions have been observed in particular with verapamil (VE) which increases propranolol bioavailability. VE increases the T1/2 of elimination and plasma digoxin concentration following single or prolonged administration. The primary mechanism appears to be renal. These modifications increase the risk of digitalis intoxication. Diltiazem (DTZ) inconsistently increases steady state plasma digoxin levels. In healthy subjects, nifedipine (NF) increases plasma digoxin concentrations and decreases digoxin renal clearance. These findings have not been observed in patients with heart failure. NF therefore leads to less marked modifications in digitalis pharmacokinetics than do VE and DTZ. Nitrendipine and nicardipine interact only slightly with digoxin, and consequently there are no pharmacodynamic effects. In healthy subjects, VE increases quinidine t1/2 and markedly decreases its metabolic clearance. Conversely, quinidine increases plasma NF levels. The primary CA are extensively metabolized by liver microsome oxidases. These result in interactions with the drugs that are also metabolized by these enzymes, or able to modify their activity. VE and DTZ decrease antipyrine and carbamazepine clearance. VE, DTZ and nicardipine lead to a marked increase in plasma ciclosporin levels. Cimetidine, but not ranitidine, increases plasma NF levels. The effects on VE are controversial. Prolonged rifampicin treatment decreases plasma VE levels.
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The effect of the new H2 receptor antagonist ranitidine on gastric pH was studied using a double-blind technique in 36 patients undergoing elective surgery, 18 of whom were given 150 mg of ranitidine orally the night before and on the morning of surgery. The incidence of gastric residue pH higher than 2.5 (p less than 0.01) was significantly greater in patients given ranitidine than in 18 untreated control patients. The mean volume of gastric aspirate in the treated group as 6.7 ml (range 2 to 20 ml) compared with the control group 15.6 ml (range 2 to 44 ml). The higher potency, longer duration of action, and fewer side effects of ranitidine compared with cimetidine suggest that this drug may have clinical advantages over other H2 receptor antagonists.
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A rat model of PD was induced by 6-hydroxydopamine. Valid PD rats were then treated with levodopa (25 mg/kg, intraperitoneally) and benserazide (12.5 mg/kg, intraperitoneally) for 21 days to induce a rat model of LID. The acute and chronic effects of administration of ranitidine at different doses (5 mg/kg, 10 mg/kg, and 20 mg/kg) on abnormal involuntary movements, levodopa-induced rotations, and the forelimb adjusting steps test were investigated in LID rats. The chronic effect of ranitidine (10 mg/kg) on the expression of Arc and proenkephalin was also evaluated.
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Fifty children (30 females; mean age 12.4 +/- 1.1 years, range 10-15 years) suffering from upper abdominal complaints and Helicobacter pylori (H. pylori)-associated gastroduodenal disease were treated with a 4 week course of ranitidine bismuth citrate (400 mg, twice daily) plus oral tinidazole (20 mg/kg) and amoxicillin (50 mg/kg) for the first 2 weeks.
Five patients with gastroesophageal reflux disease (GERD), who also had chronic functional diarrhea and postprandial urgency, unexpectedly noted rapid relief of their diarrhea and urgency when they took lansoprazole for their heartburn. To determine if this surprising result was not fortuitous, all 20 patients seen during the next six months for chronic diarrhea and postprandial urgency due to irritable bowel syndrome (IBS) or functional diarrhea were treated with inhibitors of gastric secretion: 14 with proton-pump inhibitors and 6 with H2 blockers. All patients had rapid, marked improvement. Usually within three days, their symptoms abated and they usually had one to three formed stools per day. Relief continued during the one to six months they were followed on therapy. Five patients stopped therapy, had recurrent diarrhea, and rapid relief upon resuming therapy. Thus, inhibition of gastric secretion effectively controls the diarrhea and postprandial urgency associated with IBS or functional diarrhea, probably by diminishing the gastrocolic or gastroenteric reflex.
The characteristics of histamine-stimulated adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation in slices of rabbit cerebral cortex have been investigated. The selective H2-receptor antagonists, cimetidine, tiotidine, metiamide and ranitidine appeared to antagonize the stimulation of cyclic AMP accumulation elicited by histamine in a competitive manner consistent with an interaction with histamine H2-receptors. The H1-receptor antagonist mepyramine (0.8 microM) produced only a weak inhibition of the response to histamine. The inhibition appeared to be non-competitive producing a decrease in the maximal response with little effect on the EC50 value. The specific H2-receptor agonist, impromidine, produced a maximum response of only 31 +/- 2% of that obtained with histamine. Studies with histamine and impromidine in combination indicated that impromidine was not acting as a partial agonist. 2-Thiazolylethylamine, a selective H1-agonist, produced only a weak response (EC50 approximately 1mM) yielding a relative potency with respect to histamine (= 100) of 2.5. In the presence of a supramaximal concentration of impromidine, histamine and 2-thiazolylethylamine further elevated the response to impromidine. In these conditions the relative potency of 2-thiazolylethylamine was increased to 59 (histamine = 100), a value which was comparable with that reported for H1-receptor-mediated contractions of guinea-pig ileum. The H1-receptor antagonists mepyramine, promethazine, triprolidine and chlorpheniramine competitively antagonized the potentiation of impromidine-stimulated cyclic AMP accumulation elicited by histamine and 2-thiazolylethylamine in rabbit cerebral cortex without affecting the response to impromidine alone. (+)-Chlorpheniramine was some 150 fold more potent than the (-)-isomer in this respect. Histamine and adenosine in combination had a much greater than additive effect on the accumulation of cyclic AMP in rabbit cerebral cortical slices. The potentiation of the adenosine response could be partially but not completely antagonized by either cimetidine or mepyramine. In the presence of H2-receptor blockade with 0.02 mM tiotidine, histamine elicited a significant potentiation (EC50 44 microM) of the response to adenosine. This response was antagonized competitively by mepyramine yielding a KB value of 0.05 microM similar to that obtained from inhibition of the potentiation of impromidine-stimulated accumulation of cyclic AMP (0.02 microM). These results suggest that there are two components in the response to histamine in rabbit cerebral cortical slices. The first component appears to be mediated by histamine H2-receptors while the second, mepyramine-sensitive, component has some ofthe characteristics ofan H,-receptor mediated response and requires prior stimulation of adenosine- or H2-receptors to produce its effect.
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Cells were pretreated for 10 min with chlorpheniramine maleate 10 μM (H1R antagonist), ranitidine 10 µM (H2R antagonist), GSK189254 1 µM (H3R antagonist) or JNJ7777120 10 µM (H4R antagonist), and then exposed to histamine (3 pM-10 nM) for 30 min.
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In a double-blind randomised trial, 40 patients with active gastric or duodenal ulcer were treated with a single nocturnal dose of famotidine 40 mg or ranitidine 300 mg for 4 to 8 weeks. Antacid tablets were allowed as additional treatment, only if needed, for pain relief. Endoscopy was repeated after 4 weeks, and if the ulcer had not healed at 6 and/or 8 weeks. Relief of upper gastro intestinal symptoms with which the patient presented and the number of antacid tablets consumed, if any, were recorded on weekly basis. Two patients in famotidine group and 5 patients in ranitidine group did not complete the therapy and were considered dropouts. At the end of therapy, ulcers in 100% of the patients receiving famotidine & 93% of patients receiving ranitidine were healed. This difference was not statistically significant. Relief from ulcer related symptoms was rapid in both the groups. None of the patients in either group reported side effects. Overall opinion of investigator was comparable for both the treatments; however, significantly (P = 0.0334) larger proportion (100%) of patients from famotidine group rated it as an excellent therapy compared to only 73% from ranitidine group. Famotidine provides excellent healing of ulcers and early relief of upper gastrointestinal symptoms in Indian patients with peptic ulcer.
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Included were 35 patients (median age, 59 years; 16 with limited disease and 19 with extensive disease; Eastern Cooperative Oncology Group performance status of < or = 1; median time off treatment 6 weeks) who were previously treated with CDE (n = 33), oral etoposide (n = 2), and reinduction CDE (n = 15); only one patient had received three CDE treatments of five cycles. The CDE regimen was followed by local thoracic radiotherapy in seven patients. Hematologic toxicity of grade 3 or 4, for leukopenia was 27% and 6%, for thrombocytopenia 21% and 13%, and for anemia 17% and 0%, respectively, for a total of 132 cycles. Two patients had neutropenic fever; no toxic death occurred. Nonhematologic toxicity was paresthesia CTC grade 3, diarrhea grade 4, and myalgia grade 3 in one patient each. Reversible paresthesia (CTC grade 1 and 2) in toes and fingers was reported in 69% of patients. Thirty-four patients were assessable for response: complete response in two patients, partial response in 23 patients, stable disease in eight patients, and progressive disease in one patient (response rate, 73.5%; 95% confidence interval, 59% to 88%). One patient was found to have atypical carcinoid at pathologic review and was excluded. Median time to progression was 21 weeks (range, 3 to 40 weeks). Median survival was 31 weeks (range, 6 to 112 weeks). One-year survival was 9%.
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Gastro-oesophageal reflux disease (GORD) is a very common disorder of upper gastro-intestinal motility, differing widely in severity and prognosis. Medical therapy of GORD has involved antacids, alginates, prokinetic agents and antisecretory compounds, primarily H2 receptor antagonists and proton pump inhibitors. Knowledge of the pharmacokinetics of these compounds is important, to optimise the therapeutic benefit in each patient. GORD patients are often elderly and pharmacokinetics are move variable in this group. Furthermore, they often suffer from other diseases needing medical therapy and may need a combination of drugs to heal reflux oesophagitis and relieve reflux symptoms. The ideal therapy for GORD will have linear pharmacokinetics, a relatively long plasma half-life (t1/2), a duration of action allowing once daily administration, and a stable effect independent of interactions with food, antacids and other drugs. Over-the-counter antacids and alginates are widely used, buy may affect absorption of H2 receptor antagonists like cimetidine and ranitidine. Aluminium-containing antacids may, over time, cause toxicity in patients with renal insufficiency. In the treatment of GORD, cisapride presents important advantages over earlier prokinetic compounds, with a longer plasma t1/2, low penetration of the blood-brain barrier and fewer adverse effects. The group of H2 receptor antagonists is still the most frequently use therapy for GORD. Linear pharmacokinetics make dose adjustments easy and safe. In individual patients, suppression of gastric secretion is related to the area under the plasma concentration-time curve (AUC), but there is wide interindividual variation in the effect of the same oral dose. Only with frequent administration and high doses will acid suppression approximate that of proton pump inhibitors. Tolerance, with loss of effect over time, however, is most pronounced in this situation. H2 receptor antagonists seem well suited for on-demand treatment of reflux symptoms, due to the rapid onset of effect and a decrease likelihood of the development of tolerance. Effervescent formulations provide more rapid absorption and almost immediate clinical effect. Cimetidine, however, causes interference with the metabolism of several other drugs in common use. In elderly patients elimination is delayed and in patients with renal insufficiency, dose reductions of all H2 receptor antagonists are recommended. The most effective medical therapy for any severity of GORD, particularly in severe oesophagitis, are the proton pump inhibitors. The substituted benzimidazoles (omeprazole, lansoprazole and pantoprazole), are prodrugs which once trapped and activated in the acid milieu of the gastric glands potently suppress gastric secretion of acid and pepsin. Their long duration of action, more related to the slow turnover of parietal cell H(+)-K+ ATPase molecules, allows once daily administration in most patients. Interindividual variation in bioavailability sometimes calls for higher doses or twice daily administration. Acid suppression is closely related to the AUC. Omeprazole is prone to interaction with the metabolism of other drugs, some of which may e be clinically important. Lansoprazole seems to have an earlier onset of action than omeprazole, ascribed to higher bioavailability during the first days of treatment. Proton pump inhibitors have a slow onset of action, which makes them unsuited for on-demand therapy. Clinical practice in GORD calls for the use of not one but several substances, according to the severity and symptom pattern of the patient. Pharmacokinetic optimisation in the treatment of GORD is a question of selecting the most suitable substances and administration schemes within each group. Cisapride is superior to other prokinetics in terms of longer plasma t1/2 and less toxicity. Amongst H2 receptor antagonists, the more long-acting compounds, ranitidine and famotidine, will improve acidity control througho
K-27 (RR=0.06), physostigmine (RR=0.15), pyridostigmine (RR=0.22) and tacrine (RR=0.28) significantly (p ≤ 0.05) reduced dicrotophos-induced mortality in comparison to the reference group (dicrotophos without pre-treatment), whereas ranitidine (RR=0.86) had no significant influence. The experimental oxime K-27, when given before dicrotophos exposure, conferred the best in vivo protection. This was significantly (p ≤ 0.05) more efficacious than pre-treatment with any other tested compounds. The differences in efficacy between the second best compound, physostigmine, and the less efficacious substances (tacrine and pyridostigmine) were also statistically significant.
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One hundred patients were entered in the study. Fifty patients randomly selected either received ranitidine or a placebo after simple closure. Follow up endoscopy was done at 1, 2 and 6 months. If persistence of ulcer was seen at 4 weeks, patients on placebo were converted to ranitidine and those on ranitidine were continued on the drug.
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Acetaminophen, caffeine, phenytoin, ranitidine, and theophylline are widely used in pediatric pharmacotherapy, but only very limited information is available on the pharmacokinetics of these medications in premature neonates. As pharmacokinetic studies in this population are hampered by limitations in the number and volume of plasma samples, we developed an LC-MS/MS assay for the simultaneous determination of these medications in small volume human plasma specimens for pharmacokinetic evaluations in neonates.
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The antisecretory effect of omeprazole on intragastric pH is decreased in the absence of Helicobacter pylori.
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The agreement between clinicians and patients in their assessments of the severity of reflux symptoms is poor, particularly before treatment and for more severe symptoms. Improvements in clinician-patient communication may help to bridge this gap, and greater reliance on patient assessments may be appropriate.
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Our purpose was to determine the effectiveness of ranitidine in a 24-week, multicenter, double-blind, placebo-controlled, dose-comparing study of 201 patients with psoriasis.
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The H+K+-ATPase is supposed to be the terminal step in the acid-secreting pathway in the parietal cell. Omeprazole blocks this enzyme, resulting in a marked inhibition of basal and stimulated acid secretion. With omeprazole 20 mg daily, 24-hour intragastric acidity is decreased by about 90%. Several clinical studies have now been published in which omeprazole has been compared with the H2-receptor antagonists cimetidine and ranitidine. Omeprazole in doses between 20 and 40 mg daily resulted in healing rates between 65% and 82% after treatment for 2 weeks and between 90% and 100% after treatment for 4 weeks. Treatment with omeprazole also gave faster and more pronounced pain relief. One comparative study in gastric ulcer has also been published showing healing rates equal to those with ranitidine. Placebo-controlled trials have also shown very pronounced therapeutic effect in reflux esophagitis. Omeprazole seems to be the drug of choice in Zollinger-Ellison syndrome, giving beneficial clinical effects and pronounced and long-lasting reduction in gastric acid secretion.
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Controlled, prospective pilot study including H. pylori-positive patients with gastric or duodenal ulcers or erosive gastritis, treated after failure of dual therapy (proton-pump-inhibitors or ranitidine plus amoxicillin) or for the first time. They were assigned to a one week triple standard therapy, consisting of metronidazole 400 mg bid + omeprazole 20 mg bid + clarithromycin 250 mg bid, or a newly created quadruple-regimen, which adds amoxicillin (1 g bid) to the above triple regimen. Each of the four drugs was given for 5 days. H. pylori status was checked by 13C urea breath test before and after four weeks of therapy.
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Ranitidine and cimetidine were much weaker at inhibiting antral damage when compared to their reported potencies as antisecretory agents. In marked contrast, loxtidine and AH22216 inhibited indomethacin-induced antral ulcers at doses similar to their reported potencies as inhibitors of acid secretion. Histological analysis at doses causing near maximal inhibition of macroscopic damage revealed an almost complete absence of ulcers but a large and significant increase in mucosal damage due to superficial erosions. Hourly dosing with hydrochloric acid reversed the protective effect of ranitidine, cimetidine and loxtidine on macroscopic damage and, histologically, this was associated with the widespread appearance of antral ulcers and a reduction in the proportion of mucosal damage caused by superficial erosions.
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To examine the effects of neutrophil activation after treatment with three different histamine-2 receptor antagonists.
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The pharmacokinetics of ranitidine was investigated in 11 patients with acute or end stage renal failure during haemofiltration. Each patient received 50 mg ranitidine i.v. The mean distribution and elimination half lives were 0.13 and 2.57 h, respectively. The total body clearance (CL) and volume of distribution (Vz) were 298 ml.min-1 (5.19 ml.min-1.kg-1) and 1.08 l.kg-1, respectively. About 17.1% of the administered dose was removed by haemofiltration (in approximately 20 l filtrate). Five of the patients still had some urine output and they excreted 0.1 to 11.8% of the dose in urine in 24 h. The haemofiltration clearance was 66.9 ml.min-1 at a filtrate flow rate of 86 ml.min-1, corresponding to a mean sieving coefficient of 0.78 (n = 6). As plasma concentrations were still in an effective range after haemofiltration, dose supplementation is not recommended.
The use of specific agents to heal mucosal lesions or to prevent non-steroidal anti-inflammatory drug toxicity, has focused upon two approaches: replacement of prostaglandin deficiency and inhibition of acid secretion. Acid suppression with traditional ulcer healing doses of H2-blockers is effective in healing gastric and duodenal ulcers upon discontinuation of the offending drug. In the event the non-steroidal anti-inflammatory drug must be continued, the use of H2-blockers is associated with a decrease in the healing rate. In long-term prevention studies, H2-blockers significantly reduce duodenal ulcer rates, but are ineffective in reducing gastric ulceration. More potent acid inhibition with a double-dose of H2-blockers (famotidine 80 mg daily, ranitidine 600 mg daily) may reduce the risk of gastric and duodenal ulcers. Marked acid suppression with proton pump inhibitors (omeprazole 20-40 mg, lansoprazole 30 mg daily) also appears to be very effective in healing gastric and duodenal ulcers in patients continuing the offending drug as well. An analysis of pooled data from comparative studies on omeprazole vs ranitidine, misoprostol and sucralfate shows a therapeutic advantage in favour of the proton pump inhibitor, ranging from 10 to 40%. In long-term prevention studies, omeprazole (20 mg daily) and pantoprazole (40 mg daily) have also been shown to reduce the risk of gastric and duodenal ulcers and non-steroidal anti-inflammatory drug-related dyspepsia. Current data from recent comparative studies of omeprazole (20 mg daily) vs ranitidine (150 mg daily) and misoprostol (200 microg daily) showed that, after 6 months' follow-up, the proton pump inhibitor was significantly superior to control drugs in reducing the risk both of gastric and duodenal ulcer. Misoprostol (at doses ranging from 400 microg to 800 microg/day) is an effective form of therapy for preventing non-steroidal anti-inflammatory drug-induced gastroduodenal lesions. However high-dose misoprostol only, seems adequate for the prevention of ulcer complications, mainly in high-risk non-steroidal anti-inflammatory drug users. Thus, available data are undoubtedly in favour of the proton pump inhibitors as well tolerated and effective drugs in the prophylaxis and treatment of non-steroidal anti-inflammatory drug-related mucosal lesions in the gastrointestinal tract.
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Plasma pharmacokinetics of ranitidine HCl were investigated after intravenous (i.v.) and oral (p.o.) administration of drug to six healthy foals. Twelve- to sixteen-week-old foals received 2.2 mg ranitidine/kg i.v. and 4.4 mg ranitidine/kg p.o. Concentrations of ranitidine were determined using normal phase high performance liquid chromatography. Plasma concentrations of ranitidine HCl declined from a mean of 3266 ng/mL at 5 min to 11 ng/mL at 720 min after administration. The profile of the plot of concentrations of ranitidine HCl vs. time was best described by a two-exponent equation for two foals; data for the remaining four foals were best described by a three-exponent equation. Mean values for model-independent values were: apparent volume of distribution (Vdss) = 1.46 L/kg; area under the curve (AUC) = 167,442 ng.min/mL; area under the moment curve (AUMC) = 18,068,221 ng.min2/mL; mean residence time (MRT) = 108.9 min; and clearance (Cl) = 13.3 mL/min.kg. Following p.o. administration, a two-exponent equation best described data for five foals; data for the remaining foal were best described by a three-exponent equation. Mean values of the pharmacokinetic values from the p.o. study include: AUC = 126,413 ng.min/mL; AUMC = 18,039,825 ng.min2/mL; mean absorption time (MAT) = 32.0 min; observed time to maximum plasma concentration (Tmax) = 57.2 min; maximum observed plasma concentration (Cmax) = 635.7 ng/mL; and bioavailability (F) = 38%.