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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen patients with effort angina, a positive exercise test and at least one stenosed vessel in coronary angiography were studied. Following a crossover blind-design, each patient received at random either 400 mg/day oral celiprolol or 120 mg/day oral nicardipine. A treadmill exercise test and 24 hour Holter monitoring were accomplished at the end of each treatment period. Both drugs significantly prolonged exercise time and reduced maximum ST segment depression at similar stages of control testing. Nicardipine reduced resting diastolic blood pressure a mean of 18 mm Hg (p less than 0.005) and also systolic blood-pressure 11 mm Hg (p less than 0.005) while celiprolol only reduced systolic pressure 10 mm Hg (p less than 0.01). Resting heart-rate was lowered by celiprolol a mean of 9 beats/min (p less than 0.0001) while nicardipine slightly increased it. The double product at maximum effort decreased with celiprolol and increased with nicardipine. Six patients with 3 vessel disease continued having transient ischemic episodes during treatment with celiprolol and 5 had them with nicardipine. Both drugs were well tolerated by the patients. In conclusion celiprolol and nicardipine proved to be effective in the treatment of myocardial ischemia specially when coronary heart disease is not very advanced.
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PMID:[A comparative study of celiprolol and nicardipine in stable angina of effort]. 168 17

In an open, randomized, multicenter trial, intravenous nicardipine was compared with sodium nitroprusside in 74 patients with hypertension (mean arterial pressure [MAP] greater than or equal to 100 mm Hg) following coronary artery bypass surgery. Nicardipine was administered as a 2.5- to 12.5-mg bolus followed by a 2 to 4 mg/h infusion, and nitroprusside as a 0.5 to 6.0 micrograms/kg/min infusion. The aim was to reduce MAP to less than 90 mm Hg within 50 minutes and maintain it stable at 85 +/- 5 mm Hg. Nicardipine was effective in 35 of 38 patients (92%), and nitroprusside in 29 of 36 (81%) (NS). The decrease in MAP was not statistically different, but time until reaching the therapeutic end-point was shorter with nicardipine (P less than 0.01). Significant differences follow: increase in heart rate and decreases in mean pulmonary artery, right atrial, and pulmonary capillary wedge pressures were more marked with nitroprusside (P less than 0.01 and P less than 0.05, respectively), whereas elevation of cardiac index and depression of systemic vascular resistance were more marked with nicardipine (P less than 0.01 and P less than 0.05, respectively). Postreduction MAP was more stable with nicardipine, 51% +/- 24% of readings falling within the range 85 +/- 5 mm Hg versus 41% +/- 18% on nitroprusside (P = 0.058). Dose adjustment during the following 24 hours was less frequent with nicardipine, 1.1 +/- 1.6 versus 2.7 +/- 2.6 (P less than 0.01). Transfused blood volume was lower with nicardipine (924 +/- 644 mL) than nitroprusside (1,306 +/- 901 mL) (P = 0.08), despite similar postoperative blood losses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of nicardipine and sodium nitroprusside in the treatment of paroxysmal hypertension following aortocoronary bypass surgery. 187 13

Nicardipine is a second-generation dihydropyridine calcium antagonist with relative coronary and cerebrovascular selectivity. To study the effects of nicardipine on systolic and diastolic myocardial function, we used three experimental models. In isolated feline papillary muscle, nicardipine produced a dose-dependent calcium antagonistic effect manifested by depressed indexes of contraction and relaxation. In an autoregulating blood-perfused isolated rabbit heart preparation, nicardipine markedly increased coronary blood flow and slightly decreased systolic pressure at a given end-diastolic pressure. The systolic pressure and +dP/dt versus volume curves, however, were shifted to the left during nicardipine administration, indicating improved systolic function. This increase was accompanied by decreased volume elastance and is probably due, at least in part, to the coronary turgor effect. In humans at rest, intravenous nicardipine administration produced pronounced coronary and systemic vasodilation with improved left ventricular systolic performance and enhanced relaxation accompanied by reflex sympathetic activation. With exercise to ischemia, nicardipine preserved the salutary effects on left ventricular function seen at rest and significantly blunted the increase in left ventricular end-diastolic pressure observed in the control setting. Administration of intracoronary nicardipine to patients produced a slight and transient depression of systolic and diastolic left ventricular function that was accompanied by a pronounced coronary vasodilator response and later by improved ventricular function. This improvement was manifested by decreased end-systolic volume and increased +dP/dt without changes in heart rate, arterial pressure, end-diastolic pressure, or end-diastolic volume. Global diastolic function indexes, including the time constant for isovolumic relaxation, peak filling rate normalized for stroke volume, and volume elastance, were unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of nicardipine on myocardial function in vitro and in vivo. 229 78

To define the short-term effects of intravenous nicardipine on exercise- and pacing-induced myocardial ischemia, 15 men with coronary artery disease were studied. Nicardipine was administered as a 2 mg bolus followed by an infusion, titrated to maintain a 10 to 20 mm Hg decrease in systolic arterial pressure. At rest, nicardipine significantly decreased systemic and coronary vascular resistances and left ventricular end-diastolic pressure but increased coronary blood flow, heart rate, and myocardial oxygen consumption. With bicycle exercise performed to evoke myocardial ischemia, nicardipine prolonged exercise duration, time to of 1 mm ST segment depression, and increased cardiac work to onset of angina in most patients. These changes in cardiac performance were not associated with alteration in the product of systolic pressure and heart rate or with increased left ventricular end-diastolic pressure. During increased heart rate induced by atrial pacing to cause ischemia, the heart rate threshold for myocardial ischemia was not changed by nicardipine. This occurred despite decreased myocardial oxygen consumption, unchanged coronary blood flow, and otherwise similar hemodynamic changes as those observed during exercise. However, left ventricular end-diastolic pressure remained lower and stroke volume increased more after nicardipine with pacing stress when compared with observations before nicardipine with the same heart rate stress. These findings support beneficial antiischemic actions of nicardipine with possible prevention of ischemia-related left ventricular dysfunction.
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PMID:Acute antianginal hemodynamic effects of nicardipine in coronary artery disease. 230 Dec 44

Effects of nicardipine, a dihydropyridine calcium antagonist, on regional myocardial blood flow (RMBF), myocardial oxygen tension (PO2), and excitation and conduction abnormalities during the occlusion of the left anterior descending coronary artery (LAD) were examined in anesthetized dogs, and compared with those of nifedipine and dipyridamole. RMBF was calculated from the H2 gas clearance curves, and PO2 was measured using a membrane-coated Pt wire. Excitation and conduction abnormalities during the LAD occlusion were represented in terms of the degree of ST-T alternans (STTA), TQ depression, and conduction delay, which appeared in epicardial electrograms. Nicardipine and nifedipine in a dose of 10 micrograms/kg increased RMBF and PO2 levels in nonischemic and mildly ischemic tissues, but not in severely ischemic tissues. Nicardipine in a dose of 100 micrograms/kg and nifedipine in a dose of 10 micrograms/kg attenuated the degree of STTA, TQ depression, and conduction delay observed in severely ischemic tissues. In mildly ischemic tissues where only TQ depression was observed without STTA, nicardipine in a dose of 30 micrograms/kg attenuated TQ depression. Dipyridamole in a dose of 1 mg/kg produced only a slight attenuation of STTA and conduction delay. These results suggest that the beneficial effects of nicardipine as well as of nifedipine on myocardial ischemia are due to the increase in the myocardial PO2 levels caused by the increased RMBF and also to direct protecting effects on ischemic myocardial cells. In the severely ischemic tissues, the latter is a main effect of the drugs. In increasing the PO2 level, nicardipine was similarly potent as nifedipine, but in the direct effect, nicardipine was less potent, and dipyridamole was almost ineffective.
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PMID:Effects of nicardipine, a dihydropyridine calcium antagonist, on regional myocardial blood flow, myocardial oxygen tension, and electrical abnormalities during acute coronary artery occlusion in dogs. 241 Jun 98

The effects of oral nicardipine (40 mg) and nifedipine (20 mg) in combination with atenolol (100 mg) were compared with those of placebo, oral nitroglycerin (0.4 mg) and atenolol alone (100 mg) in 17 patients with stable effort angina. Patients performed symptom-limited, multistage, upright bicycle ergometric exercises with computer-assisted ECG analysis in bipolar lead CM5. Nicardipine and nifedipine were given double blind and in randomized order. In comparison with placebo (4818 +/- 2021 kpm), patients exercised longer and with a greater work load with nitroglycerin (5748 +/- 1711 kpm, P less than 0.001), the combinations of atenolol and nifedipine (6120 +/- 2274 kpm, P less than 0.05), and atenolol and nicardipine (6671 +/- 2339 kpm, P less than 0.01), but not with atenolol alone (5305 +/- 1524 kpm, P = NS). The magnitude of ST-segment depression at peak exercise with placebo (3.22 +/- 1.72 mm) was dramatically reduced with nitroglycerin (1.39 +/- 1.87 mm) but less with atenolol alone (2.95 +/- 1.83 mm, P less than 0.05) or the combinations of atenolol and nicardipine (3.05 +/- 1.51 mm, P = NS), and atenolol and nifedipine (2.45 +/- 1.25 mm, P less than 0.001). Compared to the combination of atenolol and nifedipine, that of atenolol and nicardipine produced a significantly (P less than 0.05) greater exercise tolerance (6671 +/- 2339 versus 6120 +/- 2274 kpm) but with a greater ST-segment depression at peak exercise (3.05 +/- 1.51 versus 2.45 +/- 1.29 mm, P less than 0.01).
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PMID:Comparison of the anti-anginal efficacy of nicardipine and nifedipine in patients receiving atenolol: a randomized, double-blind, crossover study. 265 28

The stresses of the perioperative period often requires the use of vasoactive drugs for hemodynamic control. Nicardipine hydrochloride is a short-acting dihydropyridine calcium antagonist with a unique configuration and characteristics that make it attractive for intraoperative and postoperative use. Nicardipine has highly specific modes of action, producing coronary and systemic vasodilation, a reduction in coronary spasm, and cardioprotection not consistently seen with other calcium antagonists. It produces a rapid decrease in blood pressure without severe hypotension, sinus arrest, cardiac depression, or clinically significant tachycardia, while it increases myocardial contractility and cardiac output. Nicardipine dilates the cerebral vasculature but does not significantly increase cerebrospinal fluid pressure in surgical patients without intracranial lesions. Unlike nifedipine, which must be administered orally or sublingually, nicardipine is stable in parenteral formulation ("light stable and water soluble") and can be given intravenously. The distinctive characteristics of nicardipine suggest that anesthesiologists might find it preferable to other vasodilators or calcium antagonists for hemodynamic control during and after surgery.
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PMID:The role of nicardipine during anesthesia and surgery. 265 8

The systemic and coronary hemodynamic effects of nicardipine, a calcium antagonist, were studied in 30 patients. Increased coronary blood flow (from 102 +/- 9 to 147 +/- 13 ml/min; p less than 0.001), heart rate (from 69 +/- 3 to 81 +/- 3 beats/min; p less than 0.001), stroke volume (108 +/- 6 to 123 +/- 6 ml; p less than 0.001) and cardiac output (from 7.3 +/- 0.5 to 9.9 +/- 0.5 liters/min; p less than 0.001) were demonstrated in 15 patients administered intravenous nicardipine (2 mg bolus given over 1 minute, followed by infusion of 50 micrograms/min to maintain 10 to 20 mm Hg decrease in systolic blood pressure). Systemic vascular resistance decreased (from 1,183 +/- 70 to 733 +/- 33 dynes s cm-5) as did coronary resistance (from 1.47 +/- 0.1 to 0.7 +/- 0.1 mm Hg/ml/min; p less than 0.001). Other hemodynamic parameters such as left ventricular end-diastolic pressure, stroke volume and work, aortic blood flow and acceleration, ejection and external power, myocardial oxygen consumption and time constant for left ventricular isovolumic relaxation also were evaluated. To distinguish between direct myocardial effects of nicardipine and peripheral effects, 15 patients were given intracoronary nicardipine (0.1 or 0.2 mg) during cardiac catheterization. Nicardipine produced slight depression of left ventricular contractile function and impairment of left ventricular relaxation; but these changes were mild and transient compared with the marked and sustained increase in coronary blood flow that persisted 7 minutes after administration. Thus, nicardipine is a relatively selective vasodilator with minimal direct myocardial depressant activity n humans.
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PMID:Effects of intravenous and intracoronary nicardipine. 280 74

Nicardipine was found to produce a concentration-dependent depression of the isometric contraction of the isolated, spontaneously beating atria of the guinea-pig. It also depressed the atrial rate of the isolated, spontaneously beating atria of the guinea-pig. The effect of the increasing concentrations of nicardipine on the heart rate was negligibly weaker than its effect on the isometric contraction. A time-dependent depression of the isometric contraction and the atrial rate after the addition of a single dose of nicardipine was also found up to the 10th min. Calcium almost completely, isoprenaline completely and aminophylline partially antagonized the depressive action of nicardipine on the isometric contractility of the atria. Only isoprenaline antagonized the negative chronotropic action of higher doses of nicardipine. It is possible that these substances restore the contractility by compensating the calcium balance, previously changed by nicardipine, or by producing an increase in the intracellular cAMP content (isoprenaline and aminophylline).
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PMID:[Effects of nicardipine on the spontaneous beat of isolated atria of guinea pigs]. 296 60

Nicardipine, a new calcium channel blocking drug of the dihydropyridine family, was administered to 63 patients at a dose of 30 or 40 mg 3 times daily in a multicenter, randomized, double-blind, placebo-controlled, crossover trial. Nicardipine midly increased heart rate (HR) at rest and midly decreased the blood pressure (BP) at rest. When generally similar responses to the 30- and 40-mg doses were averaged, nicardipine produced a 7% increase in peak exercise HR, which was balanced by a 6% decrease in peak exercise BP. Thus, no change occurred in the exercise HR-BP product. With nicardipine, treadmill exercise duration increased 9%, time to angina increased 15%, time to 1-mm ST-segment depression increased 16%, and oxygen consumption at peak exercise increased 13%. Mean anginal frequency declined, as did mean weekly sublingual nitroglycerin consumption, but not significantly. There were more cardiovascular side effects with nicardipine than with placebo, with at least 3 patients having increased angina judged by investigators as probably related to the drug. Vasodilatory side effects were also more frequent with nicardipine, but were generally mild and well tolerated; the drug had to be discontinued in only 1 patient, because of vasodilatory effects. Nicardipine is effective and generally well tolerated in patients with chronic stable angina.
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PMID:Efficacy and safety of nicardipine for chronic, stable angina pectoris: a multicenter randomized trial. 309 55


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