Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Verapamil and nifedipine, two calcium-antagonist drugs, were evaluated in a double-blind cross-over trial. The study was performed in 15 patients admitted to our Coronary Care Unit for spontaneous angina. Before and after a 24 hours placebo period, oral verapamil 480 mg daily and oral nifedipine 60 mg daily were administered alternatively. Symptomatic as well as asymptomatic ischemic episodes with ST segment elevation or depression and ventricular and supraventricular ectopic beats were documented by continuous electrocardiographic Holter monitoring. The average number of attacks during the placebo periods was 243; the number of attacks decreased to 129 during verapamil treatment (P less than 0.05) and to 57 during nifedipine treatment (P less than 0.01). Ventricular ectopic beats decreased with both drugs while supraventricular ectopic beats decreased only during verapamil treatment. The difference was not statistically significant because of a small number of observations. In conclusion the two drugs appear to be effective in the management of patients with unstable angina at rest, especially in the variant form.
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PMID:Effects of oral calcium-antagonists in spontaneous angina. Verapamil and nifedipine in a double-blind cross-over trial. 675 85

Because severe muscular weakness was noted in animals receiving verapamil in doses exceeding those used in humans, we studied the effects of verapamil on neuromuscular function and its correlation with myocardial conduction. The flexor carpi radialis and its nerves were surgically exposed in mechanically ventilated dogs during pentobarbital anesthesia. Indirect and direct electrical stimulation was applied and twitch height recorded following the intravenous administration of verapamil. Twenty animals received one of four dose schedules. The results showed a significant dose-related depression of twitch height to indirect stimulation. Twitch height to direct stimulation was reduced only with the highest dose. The onset of depression of indirect stimulation was temporally associated with onset of A-V conduction delay. However, recovery following indirect stimulation lagged behind recovery of the ECG by 30 min. Recovery times of twitch height following indirect stimulation ranged from 60-208 min and also were dose-related. The qualitative similarity of pancuronium and verapamil on indirect twitch height suggests a similar site of action, i.e., the neuromuscular junction. A presynaptic or postsynaptic effect of verapamil could not be discerned in this study. Verapamil may produce an unrecognized source of weakness in the anesthetized patient either alone or through interaction with anesthetic agents or adjuncts.
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PMID:Neuromuscular and electrocardiographic responses to verapamil in dogs. 684 9

Electrophysiologic evaluation before and after the serial administration of verapamil, lidocaine, propranolol, and procainamide was undertaken in 4 young, asymptomatic patients with recurrent, sustained ventricular tachycardia (VT). No patient had obvious organic heart disease. The electrocardiogram during sinus rhythm showed S-T depression and T-wave inversion over the inferior and lateral precordial leads in 3 patients. QRS morphologic characteristics during episodes of VT showed a pattern of right bundle branch block and left axis deviation. In all 4 patients, VT could be both induced and terminated with electrical stimulation. Verapamil terminated VT and prevented the induction of sustained VT in 3 patients, and markedly slowed the rate of VT in 1 patient. Procainamide effectively prevented the induction of sustained VT in 2 patients, and although ineffective in preventing induction in 2 patients, it slowed the rate of tachycardia in both. Lidocaine and propranolol did not prevent the induction of VT in any patient. These findings suggest that slow-response tissues may be involved in the genesis of VT in these patients, and that VT in these patients may represent a unique clinical entity with distinct electrocardiographic, electrophysiologic, and electropharmacologic properties.
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PMID:Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: a unique clinical entity with specific properties. 685 37

The relative efficacy of two calcium antagonist drugs, verapamil, 120 mg three times a day and nifedipine, 20 mg three times a day, was examined in a double-blind randomised trial. Patients were assessed at the end of four week periods by a maximal treadmill exercise test, the frequency of anginal attacks, glyceryl trinitrate consumption, and side effects. Sixteen point praecordial maps were recorded at rest, immediately after exercise, and at minute intervals for 10 minutes. Total ST segment depression (epsilon ST) was used as a measure of myocardial ischaemia. Both verapamil and nifedipine increased maximal work capacity but epsilon ST at the termination of the test remained constant. Both drugs reduced the frequency of anginal attacks and glyceryl trinitrate consumption. Systolic blood pressure at rest and on exercise was reduced by both drugs. Verapamil and nifedipine were equally effective in treating angina, but side effects were more common with nifedipine.
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PMID:Calcium antagonist drugs in chronic stable angina. Comparison of verapamil and nifedipine. 703 54

In 18 patients with stable effort angina, verapamil, 80 mg four times daily, was compared with propranolol, 80 mg four times daily, in a double-blind, placebo-controlled trial to assess the effects on anginal threshold, exercise capacity and left ventricular function measured by gated equilibrium blood pool scanning. Both propranolol and verapamil improved exercise capacity (placebo 424 +/- 135 W-min; propranolol 513 +/- 168 W-min, p less than 0.01; verapamil 545 +/- 215 W-min, p less than 0.005) and prolonged the time to 1 mm of ST depression (placebo 4.5 +/- 1.3 minutes; propranolol 7.4 +/- 1.4 minutes, p less than 0.005; verapamil 6.6 +/- 1.9 minutes, p less than 0.005). At rest, the mean left ventricular ejection fraction did not change significantly during drug therapy (placebo 57 +/- 13%, propranolol 55 +/- 12%, verapamil 55 +/- 13%). While taking placebo, all 18 patients had a decrease in exercise ejection fraction. In contrast, 12 patients taking propranolol and 14 patients taking verapamil had a 5% or greater increase in ejection fraction during exercise. Verapamil is an effective primary therapy and a satisfactory alternative to propranolol in patients with stable effort angina.
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PMID:A double-blind randomized trial of propranolol and verapamil in the treatment of effort angina. 704 90

A 35-year-old man with class 2 angina pectoris was enlisted in a serial exercise test protocol to evaluate oral verapamil therapy for angina pectoris. During both the single-blind open dose titration phase and the double-blind phase, short salvoes of ventricular tachycardia (VT) were followed by angina and ischemic ST segment depression during exercise with placebo. With verapamil therapy, no ventricular ectopy was noted during exercise, and the patient exercised longer before angina or ischemic ECG changes developed. Twenty-four hour ECG monitoring revealed multiform ventricular premature depolarizations and three-beat salvoes of VT with placebo and no ventricular ectopy whatsoever with verapamil. Verapamil's antiarrhythmic effect may be secondary to its anti-ischemic action, or, by inhibiting slow channel conduction (with its propensity for enhanced automaticity and reentry) induced by ischemia and the sympathetic response to exercise, exerts a primary antiarrhythmic action.
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PMID:Suppression of ischemic related ventricular tachycardia by verapamil during treadmill exercise testing. 708 17

Two patients with classical effort-induced angina pectoris associated with abnormal ST-segment depression on graded exercise testing and normal coronary arteriograms are described. Both patients deteriorated during treatment with propranolol, and became asymptomatic during treatment with verapamil with normal graded exercise tests. Verapamil may thus improve an inadequate vasodilatatory response of the coronary vascular bed to effort.
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PMID:Verapamil in effort-induced angina pectoris in patients with normal coronary arteries. 710 8

The effects of phentolamine on rabbit basilar artery were studied and compared with those on other smooth muscles. The drug showed a dose-dependent depressing effect on high-potassium-induced contracture of rabbit basilar artery. The depressing effect was stronger on tonic than on phasic contraction. When phentolamine was applied during high-potassium-induced tonic contraction, dose-dependent relaxation was observed. The degree of phentolamine-induced-relaxation of high-potassium-induced tonic contraction was not affected by surgical denervation of the basilar artery, although catecholamine content was almost completely lost, as indicated by chemical and histochemical experiments. The relaxed tension caused by phentolamine was reversed by addition of Ca in a dose-dependent manner. Verapamil also showed a dose-dependent relaxing effect on high-potassium-induced contracture, with this relaxed tension being reversed by the addition of Ca in a dose-dependent manner. The relaxing effect of phentolamine on rabbit basilar artery was stronger than on rabbit aorta or guinea-pig taenia coli. Phentolamine depressed serotonin- or histamine-induced contraction at a concentration more than 10 times higher than the concentration for depression of noradrenaline-induced contraction. The depression of high-potassium-induced contracture and reversal by additional Ca, especially in denervated preparations, indicates that phentolamine acts directly on smooth muscle in a similar manner to that of Ca antagonists.
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PMID:The direct inhibitory action of phentolamine on the contraction of rabbit basilar artery. 718 56

We evaluated efficacy and mechanisms of the antiarrhythmic action of verapamil in 20 patients with sustained supraventricular tachycardia. Two patients had sinus nodal re-entrant tachycardia, nine atrioventricular (AV) nodal re-entrant tachycardia, and nine AV reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. The study design comprised a double-blind, randomized, cross-over phase using a 0.075 mg/kg dose of verapamil versus placebo and an open-label phase using a 0.15 mg/kg dose of verapamil. The overall results of both phases showed that 15 of 19 patients converted to sinus rhythm with verapamil while only one of 16 converted to sinus rhythm with placebo. The effective plasma verapamil concentration measured 123 +/- 40 ng/mL (mean +/- SD). Verapamil suppressed sinus nodal and AV nodal re-entry but exerted no selective depression between fast and slow AV nodal pathways. It had no significant effect on accessory AV bypass tract but was effective in terminating AV reciprocating tachycardia by its depressive action on the AV node.
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PMID:Intravenous verapamil for termination of re-entrant supraventricular tachycardias: intracardiac studies correlated with plasma verapamil concentrations. 721 75

Atrioventricular (AV) conduction was studied in isolated, perfused rabbit hearts. Total AV interval was subdivided into the intraatrial, intranodal and His-Purkinje conduction times. Concentrations of Ca, K and Na in the control perfusate were 2.4, 4.5 and 144.8 mM, respectively. Generalized ischemia or hypoxia almost selectively depressed intranodal conduction, engendering a second degree block. Low Ca (0.8 mM) slightly prolonged the intranodal conduction time, whereas high Ca (4.8-7.2 mM) caused a greater prolongation of this interval, often causing intranodal block. High Ca-induced depression of intranodal conduction was antagonized by high K (7.5 mM). Verapamil (0.5-1.0 mg/L) produced a second degree intranodal block. Subsequent elevation of Na concentration to 172 mM (but not high Ca) restored a 1:1 conduction. Tetrodotoxin (2-10 mg/L) did not affect, whereas low Na (108.6 mM) severely depressed intranodal conduction. These results suggest that (1) AV nodal conduction is most vulnerable to reduced oxygen supply, (2) an optimal Ca concentration for AV nodal conduction exists, (3) high K counteracts high Ca-induced depression of AV nodal conduction, and (4) slow Na current may play a major role in generating AV nodal action potentials. Voltage clamp experiments on the AV node substantiated some of these observations.
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PMID:Peculiarities of AV nodal conduction and the role of slow Na current. 721 99


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