Autoradiographic Determination of Cerebral Glucose Content, Blood Flow, and Glucose Utilization in Focal Ischemia of the Rat Brain: Influence of the Plasma Glucose Concentration

Abstract

Summary: Focal cerebral ischemia was produced by oc clusion of the middle cerebral artery in rats, Cerebral blood flow measured with [14C]iodoantipyrine was se verely reduced in the lateral portion of neostriatum. This area of dense ischemia was sharply demarcated against the surroundings. The adjacent cortex was perfused at one-third of normal, whereas blood flow in the medial neostriatum was only slightly reduced. This pattern of perfusion was independent of the plasma glucose concen tration of the animal. In contrast, the glucose utilization calculated from the 2-pH]deoxyglucose accumulation de pended on the plasma glucose concentration. Enhanced glucose utilization was evident in the border areas sur rounding the ischemic focus in normoglycemic animals. Neither acutely nor chronically diabetic animals had such an increase of metabolism in the borderzone. Moderately hyperglycemic rats had a narrow rim of enhanced glucose Occlusion of the middle cerebral artery (MCA) causes nearly complete ischemia in the center of the vascular territory. The ischemic area is sur rounded by tissue with reduced flow and a pe riphery with almost normal perfusion. In rats, the cerebral blood flow is severely reduced in the lat eral part of the striate body, whereas the adjacent cortex reveals flow values about one-third of normal (Nedergaard et aI., 1986). Earlier, we have

Hippocampal CA3Lesion Prevents Postconcussive Metabolic Dysfunction in CA1

“…12, No.6, 1992 mllIOO g/min. Consequently, although CBF appears to be reduced during the acute period and could alter the measured LCMR g lc, even in a F-P more severe than that reported in the current study, CBF does not reach ischemic levels (Nedergaard et al, 1988).…”

Impaired Wound Healing after Cerebral Hypoxia—Ischemia in the Diabetic Mouse

“…The increased cell death after stroke observed in the diabetic patients and in several different rodent models of diabetes has been consistently attributed to the excess accumulation of lactic acid, acidosis, and reduced recovery of affected tissue (Folbergrova et al, 1992;Siesjo, 1988). However, studies by Nedergaard and Diemer (1987) and Nedergaard et al (1988) showed that preischemic hyperglycemia associated with diabetes elicited greater tissue loss after MCAO than in control animals made equivalently hyperglycemic, suggesting factors other than simple lactoacidosis are involved. This hypothesis was further supported by our own studies in db/db mice, in which we found higher levels of circulating glucose and longer durations of lactoacidosis in diabetic female db/db mice than their male counterparts despite finding the volume of the infarct was substantially smaller in the female mice (Vannucci et al, 2001).…”

The Effects of Oxiracetam (CT-848) on Local Cerebral Glucose Utilization after Focal Cerebral Ischemia in Rats.

“…However, blood glucose was in creased in the MCA-occluded group as com pared with the sham-operated group, and ox iracetam minimized this increase dose-depend ently. (19,20) have demonstrated that MCA occlu sion induced LCGU reduction in rat brain. Our study confirmed the marked reduction in LCGU; however, we found that metabolic im pairment was widespread throughout the ipsi lateral cortex.…”