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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A 69-year-old man developed acute-onset confusion and hypertension with systolic pressures in the 160s 1 day after carotid endarterectomy for right facial droop from left hemispheric lacunar infarcts. CT perfusion (figure, A-D) demonstrated findings consistent with cerebral hyperperfusion syndrome (CHS) following revascularization. CHS is caused by loss of autoregulation, hypertension, and ischemia-reperfusion injury resulting in increased regional blood flow and vascular congestion.(1) CHS following revascularization may present as ipsilateral headache, focal seizure, or neurologic deficit. Nonperfusion imaging may show intraparenchymal hemorrhage or edema. Labetalol and clonidine are used for aggressive blood pressure control until cerebral autoregulation is restored.(2.)
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The beta-adrenoreceptor blocker labetalol has demonstrated important antioxidant properties in vitro that inhibit superoxide anion production during normal leukocyte oxidative metabolism. This study investigated the in vitro and ex vivo effects of labetalol on respiratory burst in rabbit neutrophils. The production of superoxide anions was examined in activated purified rabbit neutrophils after intravenous administration of labetalol (4.0 mg/kg of body weight). At a concentration up to 200 mg/L, labetalol did not demonstrate any cytotoxic effects on neutrophils, as determined by enzyme lactate dehydrogenase activity. In the cell-free system, labetalol demonstrated no significant activity, but in formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated rabbit neutrophils, labetalol demonstrated concentration-dependent antioxidant activity. The in vitro 50% inhibitory concentration (IC50) with the fMLP stimulus was 16.5+/-0.21 mg/L in the rabbit neutrophils and 13.2+/-0.16 mg/L in the human neutrophils. In the fMLP-stimulated rabbit polymorphonuclear leukocytes, labetalol demonstrated its peak inhibitory activity (47%) 3 hours after administration. The mechanism by which labetalol acts in the treatment of hypertension may occur from an interaction in the signaling pathway of protein kinase C activation. The antioxidant properties demonstrated in this mechanism contribute to the drug's antihypertensive action and thus, may reduce the risk of injuries inflicted by reactive oxygen species involved in the pathogenesis of hypertension.
To study the influence of different maternal factors, including antihypertensive medication, on the outcome of pregnancy in primi- and multiparas with pregnancy-associated hypertension.
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A 40-year-old woman had pregnancy-induced hypertension, disseminated intravascular coagulation (DIC), choroidal infarction, and magnetic resonance imaging (MRI) high-signal abnormalities in the occipital regions. With successful treatment of the hypertension and spontaneous resolution of the DIC, the MRI signal abnormalities resolved, but visual acuity remained decreased because of damage to the retina and choroid. This case demonstrates that pregnancy-induced hypertension, particularly if combined with DIC, may produce infarction of the retina and choroid and persistent visual loss even if the effect of this condition on the occipital lobes is limited to reversible vasogenic edema.
Hypertensive patients with left ventricular hypertrophy (LVH) have increased cardiovascular morbidity and mortality. Experimental studies indicate the importance of both the alpha and beta components of the adrenergic nervous system in the development and reversal of LVH. Therefore labetalol (L), a combined alpha and beta blocker, and propranolol (P), a nonselective beta blocker, were evaluated in a randomized, double-blind study of 35 hypertensive patients with echocardiographic evidence of LVH. Following 2 weeks of placebo, L or P was titrated as needed and tolerated to maximum total daily doses of 1600 mg and 640 mg, respectively. A thiazide diuretic was added if necessary for blood pressure control. M-mode echocardiograms were performed at baseline and after 1, 3, 6, and 12 months of blood pressure control. The echocardiograms were read independently by two blinded observers for end-diastolic dimension and wall thicknesses, and left ventricular mass. Fractional shortening, cardiac output, and peripheral vascular resistance were derived using standard formulas. Both drugs reduced blood pressure significantly and comparably. Significant changes in the echocardiographic measurements were observed as early as 1 month and usually persisted throughout the study. Both drugs decreased posterior wall thickness; however, only the decrease in propranolol group achieved statistical significance. Septal wall thickness was reduced by L at 3 and 12 months. End-diastolic dimension increased significantly in the L-treated group at 3, 6, and 12 months of therapy, whereas P had no effect on this measurement.(ABSTRACT TRUNCATED AT 250 WORDS)
A retrospective chart review was conducted at two urban teaching hospitals. Twenty-two cases were identified via ICD-9 (International Classification of Diseases, 9(th) revision) codes of discharge diagnoses over an 8-year period. Only those patients who initially presented to an ED in the postpartum period after hospital discharge were included. A standardized data tool was used to extract demographic data, signs and symptoms of preeclampsia/eclampsia, ancillary studies previously associated with eclamptic pathology, and outcome during admission.
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Mesothelial cells (MC) are the first peritoneal membrane barrier in contact with dialysate. The aim of this study was to analyze the in vitro capacity of different pharmacological agents to modify the ex vivo proliferation of MC obtained from the peritoneal effluent of patients treated with peritoneal dialysis (PD).
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In this randomized clinical trial, 60 ASA I and ASA II patients who were referred for rhinoplasty were enrolled. Patients were randomly assigned to two groups. Labetalol was given to the first and nitroglycerin to the second group of patients. Blood pressure and the amount of intra-operative bleeding during surgery and surgeon satisfaction were measured.
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In a nationally representative large data set, elevated blood pressure was observed in over 60% of the patients presenting with stroke to the ED. Elevated blood pressure was associated with an earlier evaluation; however, the use of thrombolytics was restricted to patients with ischemic stroke with SBP below 185 mm Hg.
The exercise- and drug-induced potassium shifts in pregnant women was studied. Six healthy nonpregnant women, six healthy pregnant women and four hypertensive, pregnant women on labetalol performed a bicycle exercise test. Blood samples for plasma potassium concentrations were drawn before, during and after the exercise. The exercise-induced plasma potassium increase was 0.9 +/- 0.2 mmol/l in healthy control women and 0.8 +/- 0.1 mmol/l in healthy pregnant women. In hypertensive pregnant women on labetalol the increase was 0.3 +/- 0.3 mmol/l (P < 0.01). There was a negative correlation (r = 0.941, P = 0.05) between the plasma potassium and labetalol concentration. Our results suggest that the potassium exchange during normal pregnancy is not changed. Labetalol reduced the exercise-induced plasma potassium increase which contrasts to other beta-blocking agents which usually augment the plasma potassium increase caused by exercise.
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The effects of nipradilol, a nonselective beta-blocker with vasodilator activities, on the diameter of arterioles and venules were examined in rat mesentery in vivo and were compared with those of propranolol, atenolol, labetalol, nifedipine and nitroglycerin. Topical application of nipradilol (10(-7) M and 10(-6) M) dilated the arterioles significantly to 109 +/- 2% and 112 +/- 2% of control, respectively (mean +/- S.E.; n = 9; p < 0.01), without changes in blood pressure and pulse rate. The dilator effect was comparable to that of nifedipine and nitroglycerin. Propranolol constricted the arterioles (to 86 +/- 3% at 10(-7) M; n = 9; p < 0.01), but atenolol and labetalol had no significant effects. Nitroglycerin dilated venules significantly (to 108 +/- 2% at 10(-7) M; n = 6; p < 0.01) but other drugs showed no significant effects on the tone of venules. Unlike the other beta-blockers used in this study, nipradilol has dilator effects on arterioles as have nifedipine and nitroglycerin.
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Treating pregnant women with labetalol and/or MgSO4 may influence cerebral oxygen extraction in their offspring shortly after birth.
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The selectivity of antagonistic effects of nipradilol, its four isomers and denitronipradilol, a major metabolite of nipradilol, on alpha 1-adrenoceptor subtypes in rat heart, brain and spleen were examined by radioligand binding assay with [3H]-prazosin. Pharmacological characteristics of these compounds were determined in isolated aortae from rats and guinea pigs. The order of the pKi values for alpha 1High-affinity sites in the heart, spleen and brain was SR > nipradiolol > or = RR > or = SS-RS > denitronipradilol, but the order of the pKi values for the alpha 1Low-affinity sites was different in the heart and brain. There were good correlations between the pKi values of these compounds for the alpha 1High-affinity sites and the pA2 values for the contractile inhibition of the phenylephrine-induced response in rat aorta. There was no correlation between the pKi values of these compounds for the alpha 1Low-affinity sites and the pA2 values. These results indicate that: 1) alpha 1High-Affinity sites are related to vasoconstriction mediated by alpha 1-adrenoceptors; 2) Nipradilol and its isomers possess low affinity to alpha 1-adrenoceptors; and 3) The nitroxy group in nipradilol is important for its alpha 1-blocking activity.
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Two simple and sensitive spectrophotometric methods were developed for the spectrophotometric determination of labetaolol (LBT). Both methods are based on the phenolic nature of the drug. The first method (Method I) is based on coupling LBT with diazotized benzocaine in presence of trimethylamine. A yellow colour peaking at 410 nm was produced and its absorbance is linear with the concentration over the range 1-10 microg ml(-1) with correlation coefficient (n=5) of 0.9993. The molar absorptivity was 2.633 x 10(4) l mol(-1) cm(-1). The second method (Method II) involves coupling LBT with diazotized p-nitroaniline in presence of sodium carbonate. An orange colour peaking at 456 nm was obtained and its absorbance is linear with concentration over the range 1-10 microg ml(-1) with correlation coefficient (n=5) of 0.99935. The stoichiometry of the reaction in both cases was accomplished adopting the limiting logarithmic method and was found to be 1:1. The developed method could be successfully applied to commercial tablets. The results obtained were in good agreement with those obtained using the official methods. No interference was encountered from co-formulated drugs, such as hydrochlorothiazide. The method was further extended to the in-vitro determination of LBT in spiked human urine. The % recovery (n=4) were 97.7+/-5.75 and 103.27+/-5.42 using the Methods I and II, respectively.
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The purpose of this study was to investigate the effects of labetalol on uterine blood flow and cardiovascular parameters in acutely instrumented, hypertensive gravid baboons.
This study was designed to evaluate the effects of a new beta-adrenergic blocking agent with beta 2 agonist activity (dilevalol, an R-R' isomer of labetalol) on left ventricular hypertrophy regression as seen by M-mode echocardiography. The study design was a 2:1 double blind randomization of dilevalol versus metoprolol. There was an equal blood pressure reduction in the two groups (supine diastolic blood pressure fell from 101 +/- 4.5 mm Hg to 87 +/- 13.7 mm Hg, P less than .001 in the dilevalol group, and 101 +/- 4.3 mm Hg to 87 +/- 8.6 mm Hg, P less than .01, in the metoprolol group). At the end of 2 months, there was an overall 7.5% decrease in left ventricular mass index in the 16 dilevalol treated patients (this was due to a 4.4% decrease in posterior wall thickness, end diastolic dimension increased by only 1%). Of the seven patients with an increased left ventricular mass index, all demonstrated hypertrophy regression (mean 17.14%). In contrast, no significant change in left ventricular mass was seen in the metoprolol treated group. Echocardiographic left ventricular mass index and electrocardiographic evidence of left ventricular hypertrophy (using the Sokolow-Lyons criteria and Romhilt-Estes point score) had poor correlation (r = .30 and r = .38, respectively). Resting ejection fraction increased by 5% and velocity of circumferential fiber shortening by 14% in the dilevalol treatment group (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)
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Seven solid phase sorbent materials with reversed-phase, mixed-mode interactions (ion-exchange and reversed-phase), and molecularly imprinted polymers (MIP), namely Oasis HLB, Oasis MAX, Oasis MCX, Bond Elute Plexa, Bond Elute Plexa PAX, Bond Elute Plexa PCX, and SupelMIP sorbents, were investigated. The present study was focused on the retention and elution of pharmaceutically active substances based on several analyte-sorbent interaction properties. Basic drugs, such as β-blockers (i.e., atenolol, pindolol, acebutolol, metoprolol, labetalol, and propranolol) were selected as the model compounds for this study. These compounds are frequently encountered in anti-doping tests. The extraction efficiencies of the individual sorbents were compared based on the recovery of known amounts of the targeted analytes in a metered elution volume (500 μL) in three separate elution fractions. The elution efficiency of the total amount of the target analytes on various sorbents was not appreciably influenced by the volume of eluent required for complete elution. Based on the small matrix effects and clear baseline, SupelMIP was the most suitable sorbent for urine analysis. The relative analyte recoveries of the SPE-HPLC procedure proved satisfactory for the range from 94% to 105%, with an RSD ranging from 2% to 4%. The regression equations for all of the targeted compounds exhibited excellent linearity (r(2) > 0.9991) over the range of 10 to 1000 ng mL(-1). The limits of detection and quantification for the selected β-blocker compounds in urine were in the ranges of 0.6 to 2.0 ng mL(-1) and 2.0 to 6.7 ng mL(-1), respectively.
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1 Phenylephrine (1-100 microgram/kg, intravenously) produced dose-dependent increases in heart rate and blood pressure in the pithed rat. 2 The positive chronotropic response to phenylephrine (10 microgram/kg) was reduced in a dose-dependent manner by propranolol (0.01-0.3 mg/kg), but higher doses of propranolol (up to 3 mg/kg) did not reduce the response by more than about 50%. The residual response was virtually abolished by phentolamine (0.3 mg/kg) or prazosin (3 microgram/kg). Labetalol (3 mg/kg) which has both alpha- and beta-blocking activity, also abolished the positive chronotropic response. 3 The pressor response to phenylephrine (1-30 microgram/kg) was enhanced by propranolol (1 mg/kg) and abolished by phentolamine (1 mg/kg) and prazosin (30 microgram/kg). Labetalol (3 mg/kg) reduced the response to phenylephrine by 73%. 4 Propranolol (0.3 mg/kg) completely blocked the chronotropic and vasodepressor effects of isoprenaline (0.1 microgram/kg). 5 It is concluded that phenylephrine acts on both alpha 1- and beta 1-adrenoreceptors to produce an increase in heart rate, on alpha 1-adrenoreceptors to produce vasoconstriction and on beta 2-adrenoreceptors to produce vasodilation. This latter effect is usually masked by the predominant vasoconstrictor action.
The influence of the acute and chronic administration of antihypertensive agents on blood flow to various organs which are known targets of hypertension is important in the determination of drug therapy for this disorder. In association with the frequently observed fall in cardiac output and increase in total peripheral resistance in response to acute administration, beta-blockers may induce a decrease in blood flow to the brain and kidney. However, during chronic treatment it has been widely shown that total peripheral resistance returns to pretreatment levels (except for labetalol, a beta-blocker with alpha-blocking properties) whilst renal and cerebral blood flows are unaffected. Although alpha-blockers acutely lower blood pressure and induce a baroreflex-mediated increase in heart rate and cardiac output while not affecting cerebral blood flow, during chronic treatment no change in systemic or cerebral or renal blood flow is observed. Diuretics and dietary sodium restriction, which are the most widely used therapeutic interventions, are usually well tolerated; however, in aged patients in whom renal adaptation to sodium depletion is impaired, deterioration of renal function may be observed.
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The effect of beta-adrenoceptor antagonists (BAAs) differing in lipophilicity and partial agonist activity (PAA), and a full agonist, on the dissociation constant for [125I]-(-)- iodocyanopindolol binding to beta 2-adrenoceptors (KD) has been investigated. Twelve healthy, normotensive male volunteers (mean age 22.3 y) were treated with different BAAs according to a cross-over design. The drugs used were propranolol (highly lipophilic BAA, no PAA), pindolol (moderately lipophilic BAA, strong PAA), dilevalol (highly lipophilic BAA, weak PAA) and salbutamol (full agonist). Before and after a single dose and an 8 day course of one of the drugs, blood pressure and the beta 2-adrenoceptor characteristics of mononuclear leukocytes (MNL) were determined. Between the treatment periods, there was a washout interval of 14 days. All BAAs decreased the blood pressure, but only propranolol lowered heart rate. Treatment with salbutamol decreased the diastolic and increased the systolic blood pressure and heart rate. Three hours after the single dose of any of the BAAs, a more than 2-fold increase in KD was observed, and the increase became larger after 8 days of administration (up to 3.7-fold increase). In contrast, no effect on KD was observed after treatment with salbutamol. BAAs with PAA and salbutamol induced a 30% decrease in beta 2-adrenoceptor density. It is concluded that treatment with BAAs, irrespective their lipophilicity or PAA, induces a decrease in the affinity of MNL beta 2-adrenoceptors for antagonists. This phenomenon may help to explain the contradictory relationship between the kinetics and dynamics of BAAs.
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One of the ways of individualization of treating patients with hypertensive disease (HD) is an attempt of an individual action on peripheral blood circulation depending on the initially increased pre- or postloading of the heart. The clinicopharmacological studies showed that the course treatment with low dose anaprilin decreased the pre- and postloading of the heart in HD patients, intravenous administration of isoptin (5 mg) reduced the cardiac preloading and intravenous labetalol (100 mg) decreased the cardiac postloading.
Headaches tend to improve in the majority of migraineurs during pregnancy, but some patients report a worsening of migraine and present a management challenge because of the restrictions of pharmacotherapy during pregnancy. Treatment options become even more limited for pregnant migraineurs who develop preeclampsia. Labetalol was tried successfully in reducing the frequency, duration, and intensity of migraine attacks in a pregnant woman with preeclampsia. There were no significant side effects and the patient delivered a healthy baby without complications.
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