Effects Of Intravenous Nicardipine Research Articles

Effects of intravenous nicardipine followed by oral labetalol in combination with nifedipine controlled-release tablet on severe peripartum hypertension

Effects of intravenous nicardipine followed by oral labetalol in combination with nifedipine controlled-release tablet on severe peripartum hypertension

Effects of intravenous nicardipine in Chinese patients with hypertensive emergencies

The efficacy and safety of nicardipine, a dihydropyridine calcium channel blocker, was evaluated in an uncontrolled, double-masked, randomized study of 53 patients with hypertensive emergencies. Either nicardipine by intravenous bolus followed by constant intravenous infusion for 24 hours (<30 mg/h) (group I, n = 14) or nicardipine by constant intravenous infusion for 24 hours (<30 mg/h) (group II, n = 39) was assigned in a 1:3 ratio. Groups I and II both showed a therapeutic response (decrease in systolic blood pressure > 20 mm Hg and decrease in diastolic blood pressure > 10 mm Hg) 5 and 10 minutes after infusion, respectively. During constant intravenous infusion, blood pressure was stable in both groups. Adverse effects were transient and mild in both groups, except in one patient in group I. The present study demonstrated that the administration of nicardipine by infusion alone and by bolus and infusion are equally effective in the treatment of hypertensive emergency, with rapid onset of action and few adverse effects.

Effects of intravenous nicardipine on diastolic function in hypertensive patients with or without left ventricular hypertrophy

Effects of intravenous nicardipine on diastolic function in hypertensive patients with or without left ventricular hypertrophy

Electrophysiologic Effects of Intravenous Nicardipine on Sinus Node Function and Conduction in Humans

We conducted an intracardiac study of the electrophysiologic effects and kinetics of intravenous nicardipine (N) in 16 patients with or without impaired cardiac conduction, using a randomized, double-blind, crossover design versus placebo (P). N or P were infused intravenously over 5 min: the dose of N was 9.46 +/- 3.85 mg. Standard electrophysiologic parameters of atrioventricular (AV) conduction and sinus function were measured under basal conditions, between 10 and 25 min, and at 65 min, after beginning the first infusion of N or P, and between 10 and 25 min after beginning the second infusion of N or P. Treatment with N significantly reduced systolic (S) and diastolic (D) blood pressure (BP) at 10 min (35 +/- 19 and 25 +/- 17 mm Hg, respectively). N significantly shortened sinus cycle length (SCL), corrected sinus recovery time (CSNRT), AH interval, AV node (AVN) Wenckebach cycle length, and anterograde and retrograde effective (ERPs) and functional refractory periods (FRPs) of the AVN. Infranodal parameters were unaffected. Mean plasma N concentrations at 10 min were 18.5 +/- 7.7 ng/ml/kg and 5.3 +/- 3 ng/ml/kg at 60 min. Two patients experienced slight adverse effects (anginal pain and nausea); another with sick sinus syndrome developed a sinus pause. We conclude that intravenous N affects nodal, but not His conduction, and that it should be administered with care in the presence of SSS.

Changes in the Haemodynamic Responses to Exercise, Posture and Nitrates after Treatment of Congestive Heart Failure with an Arteriolar Vasodilator

1. Haemodynamic responses to exercise, posture and nitrates were measured before and after 8 weeks of therapy with an arteriolar smooth muscle specific calcium antagonist, nicardipine, in eight patients with congestive heart failure (New York Heart Association class II or III). 2. The acute haemodynamic effects of intravenous nicardipine before and after 8 weeks of oral therapy confirmed its vasodilating properties, with similar end-points to the initial response after the 8 week period. 3. After 8 weeks of oral therapy all patients improved by one New York Heart Association class and treadmill exercise duration was significantly increased. In contrast, sitting bicycle exercise duration was not prolonged, although, at the same peak workload, changes in cardiac output, stroke volume and systemic vascular resistance were significantly improved after 8 weeks of therapy. 4. Sublingual glyceryl trinitrate predominantly affected pulmonary vascular resistance before and after chronic therapy with nicardipine, although the effects were less marked after 8 weeks. In contrast, the systemic vascular effects of glyceryl trinitrate were significantly increased after 8 weeks of therapy with nicardipine. 5. Increased vasodilator responses to sublingual glyceryl trinitrate and exercise after chronic treatment with nicardipine, in the absence of significant residual vasodilatation at rest, suggests that indirect changes in systemic arterioles may accompany and possibly contribute to the clinical improvement in heart failure.

Cardiovascular effects of and interaction between calcium blocking drugs and anesthetics in chronically instrumented dogs. III. Nicardipine and isoflurane.

To assess the interaction between isoflurane and the new calcium channel blocker, nicardipine, mongrel dogs were chronically instrumented to allow the following measurements: aortic, left ventricular and left atrial pressures; heart rate; cardiac output; and carotid, coronary, and renal blood flows. The hemodynamic effects of intravenous nicardipine 5, 10, 30, and 50 micrograms/kg were measured in awake dogs and during 1.6 and 3.0 per cent (end-tidal) isoflurane anesthesia. Nicardipine induced a dose-dependent fall in mean arterial pressure in both awake dogs and during 1.6 and 3.0 per cent isoflurane anesthesia. Heart rate and cardiac output were increased in proportion to the nicardipine dose in the awake dogs and, to a lesser degree, in the dogs anesthetized with 1.6 per cent isoflurane, but did not change during 3.0 per cent isoflurane anesthesia. Left atrial pressure was unchanged by nicardipine in awake dogs and during anesthesia. Left ventricular maximum rate of tension development (dP/dt) increased in awake dogs and decreased during anesthesia. Coronary blood flow increased dose dependently without anesthesia, and, to a smaller degree, during anesthesia. Nicardipine increased carotid blood flow without anesthesia, whereas it was unchanged during anesthesia. Renal blood flow was unchanged in awake dogs and decreased during anesthesia. The authors conclude that nicardipine is a potent vasodilator that minimally affects cardiac function and regional blood flow in the presence of isoflurane. The interactions between nicardipine and isoflurane are mainly the result of the isoflurane-induced inhibition of the reflex tachycardia elicited by nicardipine.

Effects of nicardipine on coronary blood flow, left ventricular inotropic state and myocardial metabolism in patients with angina pectoris.

The effects of intravenous nicardipine (2.5 mg) on the left ventricular (LV) inotropic state, LV metabolism, and coronary haemodynamics were analysed in 22 patients with angina pectoris. Measurements were made at fixed heart rate (atrial pacing), under basal state, and during a cold pressor test. After nicardipine, coronary blood flow and oxygen content in the coronary sinus increased significantly. The indices of inotropic state increased slightly, and the rate of isovolumic LV pressure fall improved. Myocardial oxygen consumption was unchanged despite the significant reduction in pressure-rate product, but LV lactate uptake increased, particularly during the cold pressor test. When nicardipine was administered after propranolol, the indices of inotropic state were unaffected. The lack of direct effect of nicardipine on LV inotropic state was further confirmed by intracoronary injection of 0.1 and 0.2 mg in a separate group of 10 patients. It is concluded that the nicardipine-induced coronary dilatation seems to improve perfusion and aerobic metabolism in areas with chronic ischaemia, resulting in reduced lactate production and augmented oxygen consumption.