SUMMARY Cerebral metabolic rate for glucose (CMRG) was measured using the 14 C-deoxyglucose technique in a stroke model of the gerbil produced by bilateral common carotid artery occlusion. During 30 minutes of ischemia, 14 C-deoxyglucose uptake in the brain was increased along the border zone between the ischemic and nonischemic area and decreased in the ischemic areas. During the early stage of reperfusion (2 or 3 to 30 minutes), CMRG increased 50 to 150% in the cerebral cortex, caudoputamen and thalamus and 270 to 320% in the hippocampus, globus pallidus and amygdala. During the late stage of reperfusion (15 to 45 minutes), heterogeneity of CMRG appeared in the cerebral cortex, caudoputamen and thalamus. CMRG decreased to less than 50% of the control value in the cerebral cortex but remained at 200 to 300% of control in the hippocampus, globus pallidus and amygdala. The latter structures exhibited a larger and more protracted increase in glucose metabolism than the other structures most probably due to the histological vulnerability to ischemia of these structures. The relationship between the transient increase of the glucose metabolism and cell function is discussed. Stroke, Vol 14, No. 4, 1983 CEREBRAL TISSUE OF MAMMALS is highly vulnerable to both anoxia and ischemia. There are reports of reversibility in the neurological, electrical and chemical function during the period of reoxygenation or reperfusion after a certain period of insult. 1-4 The degree of reversibility has been found to depend on a number of factors. 5 -6 A better understanding of this reversibility may be important in the treatment of cerebral anoxia or ischemia since there is frequently reoxygenation or reperfusion of the brain following cerebral embolism, cardiac arrest or intoxication by various poisons.Prior to the introduction of the 2-deoxyglucose technique for the measurement of regional cerebral glucose consumption by Sokoloff, et al,7 only global techniques existed for measuring glucose metabolism. Consequently, regional alterations in metabolism could not be seen. The employment of the 2-deoxyglucose technique in the study of cerebral ischemia or anoxia may lead to an extended knowledge of cerebral damage following this type of insult.Our laboratory has previously reported measurements of regional cerebral glucose metabolism following focal cerebral ischemia in cats.8 Diemer, et al 9 have recently examined glucose utilization following total ischemia in rats. There are few studies in the literature, however, dealing with the reperfusion period following a stroke in an experimental animal.
2In the present studies a stroke model in the gerbil utilizing bilateral carotid occlusion has been utilized. In this model, all animals develop severe neurological deficits and the severity of cerebral ischemia is rather uniform from animal to animal.10 " This uniformity allows for the precise evaluation of the course following reperfusion.
MethodsMale monogolian gerbils (60-100 gm) were anesthetized with ketamine (5 mg/100 gm body weigh...