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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of blood platelets in ischemia- and reperfusion-induced arrhythmias and the efficacy of three calcium blocking drugs (verapamil, diltiazem, and nicardipine) in preventing the arrhythmias were investigated. Using anesthetized rats, we measured platelet count (Pc) continuously in vivo with a Technicon autocounter. Thromboxane B2 (TxB2) and 6-keto-PGF1 alpha levels in blood from coronary sinus were determined by radioimmunoassay (RIA). Myocardial ischemia and arrhythmias were monitored from lead I ECG during and after occlusion of the left anterior descending coronary artery (LAD) for 7 min. Ischemia-induced arrhythmias were mainly ventricular ectopic contractions (VECs), whereas reperfusion produced VECs, ventricular tachycardia (VT), and reversible and irreversible ventricular fibrillation (VF). Both ischemia and reperfusion decreased platelet count and increased TxB2 level in blood from the coronary sinus. The effects of the CEBs were determined at two dose levels (0.1 and 0.3 mg/kg). Each calcium entry blocker (CEB), at both dose levels, significantly inhibited ischemia-induced arrhythmias. Verapamil and diltiazem significantly reduced reperfusion-induced VECs, prevented VT and irreversible VF, and reduced the number of animals with reversible VF. Nicardipine in preventing arrhythmias was not very effective at either dose. The CEBs also inhibited both ischemia- and reperfusion-induced decreases in PC with a moderate increase (up to 7%) as compared with levels in sham-operated controls. The CEBs also significantly reduced TxB2 levels in blood from the coronary sinus. These results indicate that ischemia and postischemic reperfusion both induce platelet aggregation in rats. Aggregating platelets release biologically active substances including thromboxane A2 (TxA2) which exacerbates existing ischemia and facilitates generation of arrhythmias. CEBs inhibit platelet aggregation and TxA2 release and enhance PGI2 synthesis, thereby preventing arrhythmias.
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PMID:Occlusion and reperfusion-induced arrhythmias in rats: involvement of platelets and effects of calcium antagonists. 169 43

The effects of nilvadipine, a dihydropyridine type calcium channel blocker, on cerebral infarction induced by focal brain ischemia was studied in rats. The area of infarction was measured 24 hr after occlusion of the middle cerebral artery (MCA) in spontaneously hypertensive rats using triphenyltetrazolium chloride. Nilvadipine, given immediately after MCA occlusion, reduced the area of infarction significantly at doses of 0.32 mg/kg (i.p.) and 3.2, 10 and 32 mg/kg (p.o.). Nicardipine suppressed the area of infarction at a dose of 32 mg/kg (p.o.). The results suggest that nilvadipine is effective against ischemic brain injury.
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PMID:Nilvadipine, a new calcium channel blocker, reduces ischemic brain injury in rats. 174 95

Nicardipine i.v. bolus (5 mg/5 min) was administered in the pulmonary artery trunk in 13 patients (2 f, 11 m), mean age 48 +/- 8 yrs, affected by ischemia congestive heart failure, with pulmonary hypertension (pulmonary vascular resistances greater than 6 U.W. and/or systolic pulmonary artery blood pressure greater than or equal to 60 mmHg). The vasodilatation induced by nicardipine caused a rapid improvement of all hemodynamic parameters, with a significant reduction of systemic and pulmonary pressures and resistances; in addition, cardiac output increased significantly. Even if heart rate decreased and mean right atrial pressure fell, their variation did not reach statistical significance. These beneficial effects are attributable to the vasodilator action of nicardipine on the systemic and pulmonary vascular districts. Therefore, in the hemodynamic evaluation of patients with ischemic cardiomyopathy proposed for heart transplantation, we propose the employment of nicardipine in testing the vascular reactivity in cases with secondary pulmonary hypertension.
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PMID:[Bolus nicardipine in the hemodynamic assessment for heart transplantation of patients with severe failure of ischemic origin and high pulmonary resistance]. 180 48

Effects of calcium antagonists, Nicardipine and Nilvadipine, on neurologic deficits and size of infarct were studied in the rat middle cerebral artery (MCA) occlusion model. Each drug was administered immediately after induction of ischemia, and neurologic grade was evaluated 1 to 24 hours after MCA occlusion. At 24 hours post-occlusion, size of the infarct was compared with that of the control group. In addition, evolution of cerebral infarction was studied at 6 hours and 12 hours post-occlusion by magnetic resonance imaging (MRI). In the Nilvadipine-treated group, neurologic deficits improved more rapidly and the size of infarct was significantly smaller than in the Nicardipine-treated group. MRI showed a progressive extension of cortical infarct in the untreated rat, whereas the infarct size remained unchanged in the Nilvadipine-treated rat. These results suggest the potential therapeutic usefulness of calcium antagonist for acute cerebral ischemia.
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PMID:[Ca++ antagonist and acute brain ischemia: effects of nilvadipine and nicardipine on middle cerebral artery occlusion in rats]. 181 38

The role of antifibrinolytic drugs in the management of patients with aneurysmal subarachnoid hemorrhage continues to remain uncertain. Recent controlled studies suggest that although these agents may alter the course of the illness, they confer no benefit in terms of overall outcome. Confronted with these data, clinicians in North America have radically altered their management of patients with ruptured aneurysms in the last decade. In the Timing of Surgery Study (1980-1983), 54% of patients were treated with antifibrinolytic drugs and only 32% underwent surgical clipping of the aneurysm on days 0-3 from the subarachnoid hemorrhage. In contrast, only 13% of the patients in the Randomized Trial of Nicardipine in Subarachnoid Hemorrhage (1987-1989) received antifibrinolytics, whereas 53% had early surgery (unpublished observations). Further study will be required to determine if this strategy has resulted in an improvement in overall outcome. Some observers have suggested that as effective therapy for symptomatic vasospasm evolves (e.g., with hypertensive or hypervolemic therapy or calcium antagonists), the adverse effects of antifibrinolytic drugs on brain ischemia may be ameliorated. This idea must be confirmed by further evaluation of the combined use of these treatments. In the interim, antifibrinolytic drugs, if used at all, should be used with caution, and their use should be restricted to those patients judged not to be candidates for early surgery. If therapy cannot be started before day 7 after subarachnoid hemorrhage, it should not be started at all, as the reduced rate of rebleeding after the first 7 days does not justify the increased risk of brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antifibrinolytic therapy and cerebral vasospasm. 213 47

Spontaneous hippocampal electroencephalogram (EEG) was recorded in the pyramidal cell layer (PCL) and dentate gyrus (DG) during and after ischemia produced by bilateral clamping of the common carotid arteries in cats. Hippocampal theta waves, approximately 180 degree out of phase in PCL and DG, appeared within 4.3 +/- 2.3 seconds after the onset of bilateral carotid artery occlusion and continued for more than 60 minute. These hippocampal theta waves disappeared 34.2 +/- 10.2 seconds after 4 vessel occlusion. We could not find the clear difference between the two areas in the appearance and disappearance of the hippocampal theta waves. We further investigated the effects of thiamylal, ketamine and nicardipine on the hippocampal theta waves during bilateral carotid artery occlusion. Thiamylal changed the two hippocampal theta waves to a similar pattern of EEG, which has irregular slow and fast waves, in both PCL and DG. Ketamine changed the two theta waves to irregular complex pattern of fast and slow waves and spike activity, which is independent at two areas. Nicardipine, a Ca antagonist, changed the theta waves to irregular slow waves which were similar to the pattern of EEG observed before carotid artery occlusion. These results indicate that thiamylal, ketamine and nicardipine have different effects on the ischemia of hippocampus.
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PMID:[The effects of thiamylal, ketamine and nicardipine on the hippocampal theta waves produced by cerebral ischemia in cats]. 221 23

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

To clarify the effectiveness of nicardipine, one of the dihydropyridine calcium-channel blockers, for myocardial protection during cold potassium cardioplegic arrest in pediatric cardiac surgery, a clinical trial of nicardipine (0.25 mg/L) added to potassium cardioplegic solution was performed in children undergoing surgical repair of congenital heart diseases. Twenty patients were selected to receive nicardipine cardioplegia and 13 patients received a standard potassium cardioplegia, serving as a control group. Nicardipine cardioplegia provided better cardiac performance in the early postoperative period and reduced release of the MB isozyme of creatine kinase, as determined during a 48-hour postoperative period. These results suggest that nicardipine added to cold potassium cardioplegic solution offers additional protection for the myocardium during ischemia and postischemic reperfusion in pediatric cardiac surgery.
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PMID:Clinical trial of nicardipine cardioplegia in pediatric cardiac surgery. 231 Feb 47

Post-ischemic delayed cerebral hypoperfusion (PDH) is considered to be one of the most critical factors limiting brain recovery after cerebral ischemia. This experiment was designed to determine the characteristics of PDH and the effects of nicardipine on the PDH. Twenty-four dogs underwent complete cerebral ischemia for 15 min using aortic clamping method with aorto-atrial bypass formation, and cerebral cortical blood flow (c-CBF), brain stem blood flow (s-CBF), intracranial pressure (ICP), and perfusion pressure (PP) were measured for 48h. Eight dogs (1 microgram group) received nicardipine 1 microgram.kg-1.min-1 for 4 h following 10 micrograms bolus iv injection 5 min after declamping of aorta. Another 8 dogs (2 micrograms group) received 10 micrograms + 2 micrograms.kg-1.min-1 nicardipine in the same manner as in group 1. The remaining 8 served as controls. In the control group c-CBF and s-CBF decreased to 60% and 55% of pre-ischemic values, respectively 1 hour after declamping of aorta, and returned to pre-ischemic values 10 and 6 h later, respectively, in spite of no significant changes in PP's. 1 microgram group and 2 micrograms group maintained pre-ischemic CBF value throughout the experimental period, and the values were significantly higher than in control group between 1st and 5th h post-ischemia. There were no significant differences in ICP's among the 3 groups throughout the experiment. In conclusion, PDH appears to be a phenomenon always accompanying transient complete cerebral ischemia, and it is assumed to be caused by constriction of cerebral vessels. Nicardipine improved PDH, indicating that the underlying mechanism of PDH must be related to a disorder in Ca2+ metabolism of cerebral vessels after ischemia.
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PMID:[Cerebral hemodynamics of post-ischemic delayed hypoperfusion (PDH) and the effects of nicardipine on the PDH]. 234 97


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