title: Effects of calcium channel blocker on responses of blood flow, function, arrhythmias, and extent of infarction following reperfusion in conscious baboons.
abstract: Two groups of chronically instrumented, conscious baboons were studied. The effects of coronary artery occlusion for 3 hours and reperfusion for 1 week were examined on measurements of left ventricular function, ischemic-zone wall thickness, regional myocardial blood flow, arrhythmias, and extent of necrosis. The experimental group of animals (n = 7) was treated with the calcium channel blocker nisoldipine (0.1 microgram/kg/min) from 1 hour after coronary occlusion to 3 hours after coronary reperfusion. The control group (n = 6) received the vehicle (n = 4) or saline (n = 2). The effects of coronary artery occlusion and reperfusion on arterial pressure, left ventricular systolic pressure, heart rate, and left ventricular dP/dt were similar in both groups. Systolic wall thickening was reversed to paradoxical wall thinning during occlusion in both groups, and there was no recovery to systolic wall thickening over the 1-week period in either group. There were differences in regional blood flow; during coronary artery occlusion, nisoldipine increased blood flow significantly in the endocardium and epicardium of nonischemic and ischemic zones. There was a major difference in the number of arrhythmic beats per minute on reperfusion; during reperfusion, the number of arrhythmias rose markedly in the vehicle-treated group but actually fell in the nisoldipine-treated group. The size of areas at risk, infarcts, infarcts related to the area at risk, and amount of total creatine kinase (CK) and MB-CK appearing in blood were not significantly different in the two groups. Thus, in the conscious baboon, nisoldipine administered 1 hour after coronary artery occlusion exerted a marked effect in diminishing reperfusion-induced arrhythmias and improved blood flow to the ischemic zone during occlusion but did not salvage ischemic tissue.
authors.affiliation: Department of Medicine, Harvard Medical School, Boston, Massachusetts.
authors.forename: S F
authors.initials: SF
authors.lastname: Vatner
authors.forename: T A
authors.initials: TA
authors.lastname: Patrick
authors.forename: D R
authors.initials: DR
authors.lastname: Knight
authors.forename: W T
authors.initials: WT
authors.lastname: Manders
authors.forename: J T
authors.initials: JT
authors.lastname: Fallon
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D003326:Coronary Circulation; D003331:Coronary Vessels; D003402:Creatine Kinase / Q000032:analysis; D006439:Hemodynamics; D007527:Isoenzymes; D008026:Ligation; D009203:Myocardial Infarction / Q000503:physiopathology*; D009543:Nifedipine / Q000031:analogs & derivatives / Q000494:pharmacology; D015737:Nisoldipine; D010215:Papio; D010477:Perfusion; D012039:Regional Blood Flow / Q000187:drug effects
chemical_list: D002121:Calcium Channel Blockers; D007527:Isoenzymes; D015737:Nisoldipine; D003402:Creatine Kinase; D009543:Nifedipine