Trandate is used to treat severe high blood pressure (hypertension). Lowering high blood pressure Trandate helps prevent strokes, heart attacks and kidney problems.
Other names for this medication:
Also known as: Labetalol.
Trandate is a drug which is used for treating high blood pressure. It is related to carvedilol (Coreg). Nerves that are part of the adrenergic nervous system travel to most arteries where they release an adrenergic chemical norepinephrine. The norepinephrine attaches to receptors on the muscles of the arteries and causes the muscles to contract, narrowing the arteries, and increasing the blood pressure. Trandate blocks receptors of the adrenergic nervous system. When Trandate attaches to and blocks the receptors, the arterial muscles relax, and the arteries expand, resulting in a fall in blood pressure.
Generic name of Trandate is Labetalol.
Trandate is also known as Labetalol, Normodyne.
Brand name of Trandate is Trandate.
Take this medicine with food or milk.
If you want to achieve most effective results do not stop taking Trandate suddenly.
If you overdose Trandate and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Trandate are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Trandate if you are allergic to Trandate components.
Be careful with Trandate if you're pregnant or you plan to have a baby, or you are a nursing mother.
Be careful with Trandate if you have a history of liver problems, heart problems, pheochromocytoma, diabetes, any allergies.
Do not take Trandate if you have a lung disease (asthma, COPD), advanced heart block, severe bradycardia, severe heart failure, post-CABG surgery.
This drug may make you dizzy for up to 3 hours after it is given. You should remain lying down during this time period in order to prevent falls.
You should get up slowly when rising from a seated or lying position.
Be very careful if you are driving machine.
Diabetic patients should be careful with Trandate.
Do not stop taking Trandate suddenly.
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The diagnosis at the time of treatment included radiotherapy-induced internal carotid artery pseudoaneurysms in nasopharyngeal carcinoma patients (11/23, 48%), cavernous internal carotid artery giant aneurysm (6/23, 26%) and ophthalmic segment internal carotid artery giant aneurysm (4/23, 17%). Nineteen (79%) patients passed the balloon test occlusion. In the cohort of patients that passed balloon test occlusion and underwent main trunk occlusion, there were no (0/20, 0%) permanent and no (0, 0%) transient neurological complications related to a subsequent parent artery occlusion.
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Glutamic acid decarboxylase (GAD) activity was measured in the oviduct of normal rats in diestrous and in rats ovariectomized (OVX) seven days before. OVX induced a significant decrease of GAD activity in the Fallopian tube. This effect was completely reversed by coadministration of estradiol benzoate + progesterone (E + P). Simultaneous injection of atropine, but not of alpha-methyl-para-tyrosine or labetalol, completely prevented the activation of GAD induced by ovarian sterois. Moreover, prostigmin significantly potentiated the action of E + P on GAD activity in the rat oviduct. These data clearly suggest the participation of acetylcholine in the mechanisms whereby ovarian steroids regulate GAD activity in the rat Fallopian tube.
The effect of a series of beta-adrenoceptor antagonists on cholesterol biosynthesis was studied in vitro in normal human skin fibroblasts. Some, but not all, of the drugs studied stimulated the incorporation of [2-14C]-acetate into cell sterols in a dose-dependent manner. This effect was unrelated to beta-blocking potency, selectivity for beta 1 or beta 2 adrenoceptors and partial agonistic activity of the drugs, thus ruling out a beta-receptor mediated mechanism. A positive, statistically significant correlation was found, however, between the drug lipophilicity and the stimulation of sterol biosynthesis. Propranolol, the most effective agent in increasing [2-14C]-acetate incorporation into cellular sterols, also enhanced the conversion of 3-hydroxy-3-methylglutaryl CoA (HMGCoA) into mevalonic acid, suggesting an interference of lipophilic beta-adrenoceptor antagonists with HMHCoA-reductase, the feed-back regulated rate limiting step of cholesterol biosynthesis.
Pregnancy-induced hypertension (PIH) complicates 6-10% of pregnancies. It is defined as systolic blood pressure (SBP) >140 mmHg and diastolic blood pressure (DBP) >90 mmHg. It is classified as mild (SBP 140-149 and DBP 90-99 mmHg), moderate (SBP 150-159 and DBP 100-109 mmHg) and severe (SBP ≥ 160 and DBP ≥ 110 mmHg). PIH refers to one of four conditions: a) pre-existing hypertension, b) gestational hypertension and preeclampsia (PE), c) pre-existing hypertension plus superimposed gestational hypertension with proteinuria and d) unclassifiable hypertension. PIH is a major cause of maternal, fetal and newborn morbidity and mortality. Women with PIH are at a greater risk of abruptio placentae, cerebrovascular events, organ failure and disseminated intravascular coagulation. Fetuses of these mothers are at greater risk of intrauterine growth retardation, prematurity and intrauterine death. Ambulatory blood pressure monitoring over a period of 24 h seems to have a role in predicting deterioration from gestational hypertension to PE. Antiplatelet drugs have moderate benefits when used for prevention of PE. Treatment of PIH depends on blood pressure levels, gestational age, presence of symptoms and associated risk factors. Non-drug management is recommended when SBP ranges between 140-149 mmHg or DBP between 90-99 mmHg. Blood pressure thresholds for drug management in pregnancy vary between different health organizations. According to 2013 ESH/ESC guidelines, antihypertensive treatment is recommended in pregnancy when blood pressure levels are ≥ 150/95 mmHg. Initiation of antihypertensive treatment at values ≥ 140/90 mmHg is recommended in women with a) gestational hypertension, with or without proteinuria, b) pre-existing hypertension with the superimposition of gestational hypertension or c) hypertension with asymptomatic organ damage or symptoms at any time during pregnancy. Methyldopa is the drug of choice in pregnancy. Atenolol and metoprolol appear to be safe and effective in late pregnancy, while labetalol has an efficacy comparable to methyldopa. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II antagonists are contraindicated in pregnancy due to their association with increased risk of fetopathy.
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The effects of a single intravenous bolus of labetalol (0.5 mg/kg) on the cardiovascular, hyperglycaemic and adrenocortical responses to major colonic surgery were studied in five patients. Results were compared with five patients who received the same anaesthetic and had similar operations performed but who did not receive labetalol. It was observed that labetalol reduced the rises in heart rate and rate-pressure product that occur at the time of skin incision but that it did not reduce the rise in mean arterial pressure. The rises in blood glucose and plasma cortisol were significantly less in the labetalol group after 30 minutes of surgery (p less than 0.05).
[3H]-guanfacine (N-amidino-2-(2,6-dichloro 3[3H] phenyl) acetamide hydrochloride; 24.2 Ci/mmol) has been used as a radioligand in homogenates of rat cerebral cortex. Specific binding of [3H]-guanfacine was linear with respect to tissue concentration (2.5-15 mg/ml), saturable and not markedly affected in the pH range 6.5-8.0. Analysis of the saturation of [3H]-guanfacine binding using an iterative least squares fitting procedure gave best fits to a single site model. [3H]-guanfacine binding was of high affinity (Kd 1.77 +/- 0.24 nM; n = 8) to a population of non interacting sites (nH 0.99 +/- 0.02; n = 8) with a density of 118.2 +/- 8.4 fmol/mg protein (n = 8). Highest levels of binding were achieved in cerebral cortex followed by thalamus greater than hypothalamus greater than medulla/pons greater than spinal cord greater than striatum greater than cerebellum. Binding was stereoselective with regard to the (-)-isomer of noradrenaline and the order of potency for displacement of [3H]-guanfacine by agonists was naphazoline greater than clonidine greater than (-)-adrenaline greater than (-)-alpha methylnoradrenaline greater than (-)-noradrenaline greater than (+/-)-alpha-methylnoradrenaline greater than (+)-noradrenaline greater than methoxamine greater than (+)-adrenaline greater than phenylephrine and by antagonists was phentolamine greater than dihydroergocryptine greater than piperoxane greater than yohimbine greater than prazosin greater than labetalol greater than indoramin suggested binding to alpha 2-adrenoceptors. The monovalent cations Na+ and K+ and also guanosine 5'-triphosphate (GTP) produced concentration-dependent inhibition whereas the divalent cations Ca2+, Mg2+, and Mn2+ first enhanced, then inhibited [3H]-guanfacine binding. Na+ (150 mM) or GTP (100 microM) produced marked reductions and Mn2+ (5 mM) marked increases in the number of receptor sites labelled by [3H]-guanfacine. 9 It is concluded that [3H]-guanfacine preferentially labels a high affinity state of the alpha 2- adrenoceptor in homogenates of rat cerebral cortex.
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Labetalol, an alpha- and beta- adrenoceptor antagonist was investigated for its central nervous system effects in rats and mice. A marked reduction in the spontaneous motor activity with no concomittant muscle weakness was produced. The drug caused closure of eyelids in rats. Labetalol caused hypothermia and prolonged the pentobarbitone-induced hyposis. In animals trained for conditioned avoidance response the drug blocked the SCR in all the animals and CAR in a few number of animals. The drug did not protect the animals against electroshock convulsions. From the results it appears that labetalol is a central nervous system depressant.
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The excitotoxins, kainic acid and N-methyl-D-aspartic acid (NMDA), were injected bilaterally into the paraventricular hypothalamus of rats. Kainic acid elicited pressor responses, tachycardia and sudden cardiac death in Nembutal-anesthetized rats. Injections of NMDA caused cardiovascular stimulation on cessation of halothane anesthesia. Intramyocardial hemorrhage, hyaline myocardial necrosis and predominantly mononuclear inflammation were evident 48 h following NMDA. Labetalol pretreatment did not protect from nor did i.v. NMDA cause these changes. Intrahypothalamic excitotoxin injections cause deleterious myocardial changes.
In so-called essential hypertension, at least three different subsets of pathophysiologic findings can be identified: mild hypertension in nonobese juvenile subjects characterized by elevated cardiac output, normal peripheral resistance, increased sympathetic activity as measured by norepinephrine and plasma renin activity; hypertension in the elderly with a low cardiac output, often with left ventricular hypertrophy, elevated total peripheral resistance, nephrosclerosis contracted intravascular volume, and low plasma renin activity; and obese hypertensive patients with a high cardiac output, expanded intravascular volume, and a normal total peripheral resistance. Although there is often an overlap among these three entities, antihypertensive treatment can easily be adapted accordingly. A beta-adrenoreceptor blocker is the step-one drug to be used in mild hypertension with an elevated cardiac output. The drug's negative inotropic and chronotropic properties will bring the elevated cardiac output and heart rate back to normal. In the elderly hypertensive patient, an arteriolar and venous vasodilator, such as an antiadrenergic agent, slow channel calcium blocker, or a converting enzyme inhibitor, will lower total peripheral resistance and unburden the left ventricle. In the obese patient and also in most black subjects, the first-step antihypertensive agent remains a thiazide diuretic. Labetalol, an agent with both beta- and alpha-adrenoreceptor properties, shows promise for the treatment of hypertension in the young as well as in the older patient. It seems to be the agent of choice in patients with established essential hypertension who are concomitantly suffering from coronary artery disease.
Sixty patients with chronic sinusitis and nasal polyps were divided into three groups: Sodium nitroprusside (SNP) group (A), diltiazem+SNP group (B), labetalol+SNP group (C). We started induced hypotension with beginning of functional endoscopic sinus surgery. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), cardiac index (CI) and ejection fraction (EF) were recorded during induced hypotension. Sugar and lactic acid in arterial and venous blood were also assayed. Then we calculate rate-pressure product (RPP), arteriovenous difference in blood glucose [D(v-a) BG], blood glucose extraction rate (BGER), arteriovenous difference in lactate [L(v-a)] and lactate produce rate (LPR).
Three patients are described who experienced headache from hypertension: one had acute headache from acute hypertension, one had daily, morning headaches from chronic hypertension, and one had acute headache with generalized tonic-clonic seizure from hypertensive encephalopathy. The presumed pathophysiological mechanisms involved in the three hypertensive headache conditions are reviewed.
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Fifteen patients with severe or malignant resistant arterial hypertension were treated by simultaneous administration of captopril and labetalol. Seven patients (group A) were given captopril alone and 8 patients (group B) labetalol alone without noticeable results. However, when the two drugs were given jointly a significant fall in mean arterial pressure from 165 +/- 19.8 (+/- 1 S.D.) to 102.4 +/- 15.1 mmHg (p less than 0.001) in group A patients and from 162.7 +/- 20 to 117 +/- 21.4 mmHg (p less than 0.05) in group B patients was observed. There were no significant changes in heart rate, a few side-effects were recorded. The captopril-labetalol combination may be considered as a useful alternative treatment of resistant arterial hypertension.
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The beta- and alpha-adrenoceptor blocking activity, the specificity of its beta-adrenoceptor blocking action, partial agonistic and membrane-stabilizing properties, as well as antihypertensive, antiarrhythmic, and anti-ischemic effects were studied. Proxodolol was shown to be superior to labetalol in its beta-adrenoceptor blocking action and similar to it in its alpha-adrenoceptor blocking agent. The drug has no a partial agonistic activity and produces a moderate membrane-stabilizing action. Proxodolol proved to be effective in treating experimental hypertension and arrhythmias. It exhibits anti-ischemic activity.
Complete final steady state selective antagonism by beta-blockers of different conventional classes versus acetylcholine effects on isolated frog rectus abdominis, guinea pig ileum and spontaneous beating auricles had been measured. The results do not support common beta-blockers groupings, nor binary conventional subdivision of "nicotinic" and "muscarinic" cholinergic receptors, confirming our previous findings.
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Alpha-adrenergic antagonists were the first substances to receive serious consideration as antihypertensive agents. However, their therapeutic potential in the management of essential hypertension was not realized until prazosin, a highly selective alpha 1-adrenergic antagonist, became available. A number of analogs of prazosin have now been synthesized, as have several structurally distinct alpha 1-adrenergic antagonists. Preliminary investigations suggest that these agents may also be clinically useful antihypertensive drugs. The alpha 1 receptor of arteriolar smooth muscle is the predominant adrenergic subtype determining sympathetically mediated vascular tone. Therefore, its selective blockade by an agent such as prazosin is a relevant approach to the major pathophysiologic defect in hypertension: an elevation of peripheral vascular resistance. Because prazosin has little selectivity for the alpha 2 receptor, the negative feedback control of norepinephrine release from sympathetic nerve terminals remains intact. This unique action of prazosin may explain why it effectively lowers arterial pressure without markedly increasing cardiac output, heart rate and plasma renin activity. An additional factor in the favorable therapeutic effects of this agent is its ability to induce a balanced reduction in both arteriolar and venous tone, with little change or even improvement in renal hemodynamics. The antihypertensive effects of prazosin, when used as a single agent, may be modest. However, it may be useful as initial as well as adjunctive therapy for the management of hypertension because of its high toxic to therapeutic ratio, coupled with a sustained reduction in arterial blood pressure, a low incidence of side effects, and a potentially favorable metabolic profile.
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The development of more sensitive and selective analytical techniques has greatly improved scientists' ability to study the PK, PD, and metabolism of drugs in pregnancy. This chapter has chronicled the evolution of the study of drug disposition in pregnant sheep in the laboratory. With the advent of more sensitive and selective analytical techniques, researchers have been able to progress significantly beyond measuring the extent of fetal drug exposure by a single-point determination. A number of interesting and significant advances have been made using highly selective and specific analytical techniques (i.e., gas chromatography-electron-capture detection, gas chromatography-nitrogen phosphoros-specific detection, and gas chromatography-mass spectroscopy). Researchers have characterized drug kinetics in multiple fluids from the pregnant sheep (amniotic fluid, fetal and maternal plasma and urine, and fetal tracheal fluid) and have demonstrated extensive accumulation of several basic drugs in the fluid produced by the fetal lung. With the simultaneous administration of labeled and unlabeled drug to the ewe and fetus researchers have, for the first time, examined the assumption that the clearance parameters determined from the model developed by Szeto and coworkers (1982) are not affected by the time interval between maternal and fetal infusions given on separate days. Also using SIL drug, researchers have characterized fetal hepatic first-pass drug clearance in a chronic preparation. With the establishment of a stereoselective assay for labetalol, scientists have begun to examine the fetal exposure to the individual enantiomers of racemic drugs in pregnancy. The availability of newer analytical tools and techniques (i.e., HPLC interfaced with tandem mass spectrometers) will further expand the study of drugs in pregnancy and challenge the creativity of future investigators in this field.
Twenty hypertensive patients entered a crossover, placebo-controlled study of prazosin and labetalol that was designed to compare treatment effects on blood pressure control and lipid parameters. Both drugs significantly reduced sitting and standing systolic and diastolic blood pressures (p less than or equal to 0.01). No significant differences were noted between treatment groups in total cholesterol, high-density lipoprotein cholesterol, or very low-density lipoprotein cholesterol levels. However, a trend toward an increase in low-density lipoprotein cholesterol levels was seen during therapy with labetalol, whereas in contrast, no such effect was seen during treatment with prazosin.
Cultured human umbilical vein endothelial cells oxidize low-density lipoproteins (LDL), assessed as increase in thiobarbituric acid reactive substance formation and oxidized LDL-induced cytotoxicity (lactate dehydrogenase (LDH) release). Endothelial cell-generated oxidized also enhances the adhesiveness of endothelial cells to monocytes. Carvedilol, a new vasodilating beta-adrenoceptor antagonist, inhibits the oxidation of LDL by endothelial cells and reduces oxidized LDL-induced LDH release from endothelial cells in a concentration-dependent manner with IC50 values of 2.56 and 1.38 microM, respectively. Moreover, carvedilol inhibits oxidized LDL-induced adhesion of monocytes to the endothelial cells in a similar concentration-dependent manner. Under the same conditions, propranolol, atenolol, pindolol and labetalol had only weak or no consistent effects on both LDL oxidation by endothelial cells and adhesion of monocytes to the endothelial cells. Monoclonal antibodies against human intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) or E-selectin (ELAM-1) partially blocked oxidized LDL-stimulated adhesion of endothelial cells to monocytes. The inhibitory effects of carvedilol on LDL oxidation and monocyte adhesion to endothelial cells may protect blood vessels from atherosclerotic processes associated with oxidized LDL-induced injuries.
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1 The hypotensive action of labetalol was evaluated during 24 h by continuous intra-arterial ambulatory monitoring in 14 patients. The dose used ranged from 300-1800 mg daily. 2 The drug caused a significant reduction of systolic BP in 19 and diastolic BP in 20 of the 24 h of monitoring. Heart rate was also reduced but less markedly than BP. 3 The rapid early morning increase in BP was also effectively controlled. 4 The mild pre-waking increase in BP was not significantly reduced. 5 Labetalol treatment reduced the variation in systolic BP from the lowest observed quarter-hourly mean as compared with pre- treatment values. 6 The quarter hourly mean values were consistently smooth and revealed no sudden variations which might have resulted from postural hypotension.
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The effects of dilevalol on vascular adrenoceptors were investigated using helical strips of cat arteries. In coronary arteries partially pre-contracted with prostaglandin F2 alpha (PGF2 alpha), the concentration-relaxant response curves for isoproterenol were shifted to the right by dilevalol with a potency similar to that of propranolol, although dilevalol itself did not relax the arteries. Contractions induced by norepinephrine of mesenteric arteries were attenuated by low concentrations of prazosin but were not influenced by yohimbine of up to 10(-8) M. In contrast, the norepinephrine-induced contractions of middle cerebral arteries were attenuated by yohimbine but only slightly attenuated by prazosin. With mesenteric arteries, treatment with dilevalol (10(-7) to 10(-5) M) attenuated the contractions induced by norepinephrine and phenylephrine in a concentration-dependent manner. On the other hand, contractions induced by norepinephrine and clonidine in middle cerebral arteries were not attenuated by treatment with dilevalol of up to 10(-6) M. Treatment with low concentrations of dilevalol (10(-8) to 10(-7) M) potentiated the contractile response to the electrical stimulation of adrenergic nerves in mesenteric arteries while high concentrations (3 x 10(-7) to 10(-5) M) attenuated it. The potentiation was reversed to attenuation by pretreatment with propranolol. Treatment with isoproterenol (10(-10) to 10(-9) M) also potentiated the contractile response to the electrical stimulation in the arteries. Isoproterenol did not cause any relaxation of mesenteric arteries precontracted with PGF2 alpha. Attenuations by clonidine of the response to the electrical stimulation in the arteries did not significantly differ in control arteries and those treated with a high concentration (10(-6) M) of dilevalol.(ABSTRACT TRUNCATED AT 250 WORDS)
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15 hypertensive patients presenting with diastolic blood pressures (DBP) of 130 mmHg or higher were hospitalised and treated with oral labetolol. They all received a diuretic and 400 mg of labetolol orally initially and subsequent doses at 2, 6, 12, 18 and 24 hours depending on the level of diastolic pressure. The mean of systolic/diastolic blood pressure dropped from 241/130 mmHg to 191/125 mmHg 30 minutes after the initial dose, and to 157/103 mmHg after six hours. Of the patients 73% had DBP of 115 mmHg or less six hours after the initial dose. Oral labetolol is recommended in hypertensive emergencies when sodium nitroprusside, diazoxide or trimethaphan cannot be used as an alternative to other agents.
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Hypertension (HTN) is one of the most common chronic medical conditions, affecting nearly 72 million people in the United States. A systolic blood pressure (BP) > 180 mm Hg or a diastolic BP > 120 mm Hg is considered a "hypertensive crisis." Hypertensive crises are categorized as either hypertensive emergencies or urgencies depending on the degree of BP elevation and presence of end-organ damage. The primary goal of intervention in a hypertensive crisis is to safely reduce BP. Immediate reduction in BP is required only in patients with acute end-organ damage (ie, hypertensive emergency). This requires treatment with a titratable shortacting intravenous (IV) antihypertensive agent, while severe HTN with no acute end-organ damage (ie, hypertensive urgency) is usually treated with oral antihypertensive agents. Patients with hypertensive emergencies are best treated in an intensive care unit (ICU) with titratable IV hypotensive agents. Rapid-acting IV antihypertensive agents are available, including clevidipine, labetalol, esmolol, fenoldopam, nicardipine, and sodium nitroprusside. Newer agents such as clevidipine have considerable advantages compared with other available agents in the management of hypertensive crises. Sodium nitroprusside is an extremely toxic drug, and its use in the treatment of hypertensive emergencies should be avoided. Likewise, nifedipine, nitroglycerin, and hydralazine should not to be considered first-line therapies in the management of hypertensive crises because these agents are associated with significant toxicities and/or side effects.
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Postpartum preeclampsia/eclampsia is the presence of hypertension and proteinuria, with or without seizures, occurring up to 4 weeks after delivery. We describe the Emergency Department (ED) presentation, signs and symptoms, results of diagnostic studies, management, and outcome in a cohort of patients diagnosed with postpartum preeclampsia/eclampsia at our institutions, and use this to review the diagnosis and management of postpartum preeclampsia/eclampsia.
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A patient in chronic renal failure, who was receiving large doses of the combined alpha- and beta-blocking agent, labetalol, was selected for renal transplantation. A low concentration of halothane was used for induction and maintenance of anaesthesia, but severe myocardial depression occurred which proved unresponsive to atropine or isoprenaline, although it responded to a dopamine infusion. Synergism has already been reported between labetalol and high concentrations of halothane, but this case suggests that, in patients with previous myocardial damage, much lower concentrations of this inhalational agent may prove fatal.
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