Metabolic Changes in Response to Acute Cerebral Ischemia Following Bilateral Carotid Artery Ligation in Arteriosclerotic Versus Nonarteriosclerotic Rats

Both the left and right carotid arteries of arteriosclerotic and nonarteriosclerotic male and female rats were surgically ligated to induce a state of sudden and severe cerebral ischemia. The animals promptly developed signs of cerebral impairment and were sacrificed 2, 4, 6, 8, 10, 12, 24 and 48 hours later. A similar group of animals was subjected to the same regimen of carotid artery ligation except that a week's time elapsed between the ligation of each carotid artery. As with unilateral carotid artery ligation, the bilaterally ligated animals manifested fatty metamorphosis of the liver, myocardial infarction and cerebral edema and necrosis, but the severity of these pathological changes was greatly exacerbated with the more severe ischemia. Serum creatine phosphokinase, glutamic oxalacetic transaminase, triglycerides, free fatty acids, cholesterol, glucose and corticosterone all rose dramatically and in concert with the pathological changes, e.g., fatty liver. Animals with preexisting arterial disease exhibited much greater excursions of these pathophysiological parameters during the cerebral ischemia than did animals with normal arteries. The entire response pattern indicates that cerebral ischemia is a severe stress and is capable of eliciting highly characteristic pathophysiological changes which could be used to assess the severity or course of cerebral ischemia.