Pathophysiological Responses to Acute Cerebral Ischemia in the Gerbil

The left carotid artery of healthy, male gerbils was surgically ligated to induce a state of cerebral ischemia. The animals were sacrificed two, four, six, 12, 24 and 48 hours postligation to determine whether the induced cerebral ischemia would be reflected by changes in blood chemistry. The gerbil, unlike the rat, has a well-defined circle of Willis and cerebral arterial branches which resemble the arrangement of cerebral arteries found in man. The gerbils withstood the induced cerebral ischemia relatively well with few overt signs of cerebral damage, e.g., muscular paralysis, and a low mortality rate. However, intense lipid mobilization accompanied by depletion of peripheral adipose tissue sites and fatty infiltration of the liver developed very promptly. Marked cerebral edema and definitive foci of cerebral infarction occurred in both the frontal and medial lobes of the brain. The adrenal cortices of the gerbil were markedly depleted of lipid concomitant with severe thymus gland involution indicative of intense corticosteroid release. The serum enzymes, creatine phosphokinase and glutamic oxaloacetic transaminase, both rose promptly, indicating cerebral and hepatic damage respectively. Lipids, i.e., triglycerides, free fatty acids and total cholesterol, all rose promptly and to significantly above-normal levels and remained super-normal throughout the 48-hour course of the experiment. Concomitant with the hyperlipidemia and other metabolic changes there were definite hyperglycemia and elevation of BUN levels in a brisk response to the induced, acute cerebral ischemia. The gerbil adrenal gland produces hydrocortisone predominantly. Blood levels of hydrocortisone rose quickly to super-normal levels in response to the stress of cerebral ischemia but fell to significantly below-normal levels 24 and 48 hours after carotid artery ligation. These findings demonstrate that acute cerebral ischemia constitutes a severe stress in the gerbil which is reflected, almost quantitatively, by temporal changes in such blood constituents as enzymes, lipids, glucose, and adrenal stress hormones.