Cardiovascular responses to cerebral ischemia following bilateral carotid artery occlusion in SHRSP, SHRSR and WKY rats.
Systemic arterial pressure was markedly increased in the early phase of cerebral ischemia induced by bilateral carotid artery occlusion (BCAO) in stroke-prone spontaneously hypertensive rats (SHRSP). The elevated level of arterial pressure was gradually returned to the initial level, and hypotension followed in the late phase. Severe neurological symptoms such as "ischemic seizure", dyspnea and coma were developed in the late phase. All SHRSP died within 6 hr after BCAO. The heart rate continued to increase during the brain ischemia. Cardiac arrhythmias, significant increases in plasma levels of creatine phosphokinase (CPK) and CPK-MB isozyme and disruption of myofibrils were observed after BCAO, particularly after the development of ischemic seizure. In contrast, in stroke-resistant SHR (SHRSR) and Wistar-Kyoto rats (WKY), ischemic seizure did not develop, yet all died within 8 hr after BCAO. Arterial pressures were moderately increased and never decreased to below the initial levels during the observation periods. Increases in CPK-MB isozyme activities in plasma from SHRSR and WKY were not detected. Pretreatments with propranolol and reserpine inhibited the increases in heart rate, reduced the frequency of arrhythmias and prolonged the survival time following BCAO in SHRSP. Our results indicate that cardiac dysfunction, which is a consequence of the cerebral ischemia, may be one of the causes of death following BCAO in SHRSP.
D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D002339:Carotid Arteries / Q000502:physiology*; D004562:Electrocardiography; D004798:Enzymes / Q000097:blood; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D009424:Nervous System Physiological Phenomena; D010276:Parasympatholytics / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013045:Species Specificity
D004798:Enzymes; D010276:Parasympatholytics