Metabolic Changes in Response to Acute Cerebral lschemia Following Unilateral Carotid Artery Ligation in Arteriosclerotic Versus Nonarteriosclerotic Rats

The left carotid artery of arteriosclerotic and nonarteriosclerotic male and female rats was surgically ligated to induce a state of cerebral ischemia. The animals promptly developed signs of cerebral impairment and were sacrificed 2, 4, 6, 8, 10, 12, 24, and 48 hours later to determine what dynamic pathophysiological changes attend acute cerebral ischemia. Several of the arteriosclerotic animals developed myocardial infarcts concomitant with the cerebral edema, hemorrhage, necrosis, and leptomeningitis observed in general. All of the experimental animal manifested necrosis and fatty infiltration of the liver, and their adrenal glands were hypertrophied, hemorrhagic, and depleted of lipid. Serum creatine phosphokinase and glutamic oxalacetic transaminase rose abruptly after 24 hours of cerebral ischemia. Triglycerides, free fatty acids, and cholesterol alterations were in keeping with intense lipid mobilization, dissolution of peripheral adipose tissue sites, and fatty metamorphosis of the liver. The animals also showed marked hyperglycemia and increased secretion of corticosterone. These investigations indicate that acute cerebral ischemia is a severe stress and will elicit dynamic alterations in scrum parameters such as enzymes, lipids, glucose, and the adrenocortical stress hormones. Animals with pre-existing arteriosclerosis manifest more untoward effects and greater excursion in serum metabolic parameters than nonarteriosclerotic subjects.