Triple-tracer autoradiography demonstrates effects of hyperglycemia on cerebral blood flow, ph, and glucose utilization in cerebral ischemia of rats

Abstract

Triple-tracer autoradiography was used to measure topographic changes in local cerebral blood flow, cerebral tissue pH, and local cerebral glucose utilization in hyperglycemic and normoglycemic rats, all of which had undergone occlusion of the middle cerebral artery. More severe and extensive reduction of all three variables was observed in the hyperglycemic than in the normoglycemic rats. In seven normoglycemic rats, significant reduction in local cerebral blood flow (p<0.025) was observed in the ischemic but not in the contralateral nonischemicsideat the lateral portion of the caudate nucleus and the neocortex. Tissue pH was significantly lower (p< 0.025) only at the lateral portion of the caudate nucleus in the ischemic side. No significant differences in local cerebral glucose utilization were observed when the two hemispheres were compared. In the ischemic hemisphere of five hyperglycemic rats, the caudate nucleus and the neocortex exhibited significant reduction (p< 0.025) in local cerebral blood flow, tissue pH, and local cerebral glucose utilization. Even in the nonischemic hemisphere of the hyperglycemic rats, local cerebral blood flow in the caudate nucleus and the neocortex was significantly reduced (p< 0.025) compared with the normoglycemic rats. No significant change in tissue pH or local cerebral glucose utilization was observed throughout the nonischemic hemisphere of the hyperglycemic compared with the normoglycemic rats. Tissue pH was systematically lower in the hyperglycemic than in the normoglycemic rats. The threshold level of local cerebral blood flow for tissue pH reduction was 49 ml/100 g/min with a 95% confidence interval of 46-54 ml/100 g/min in normoglycemic rats (37% of control) and 63 ml/100 gJmin with a 95% confidence interval of 58-70 ml/100 g/min in hyperglycemic rats (47% of control). The threshold level of local cerebral blood flow for local cerebral glucose hypermetabolism was 20 ml/100 gJmin with a 95% confidence interval, of 20-24ml/100g/min in normoglycemic rats (15% of control) and 30 ml/100 g/min with a 95% confidence interval of 30-49 ml/100 gJmin in hypergfycemic rats (22% of control). © 1988 American Heart Association, Inc.