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Department of Neurology (Drs. Yip, Garg, and Hogan), Medical University of South Carolina, Charleston, SC; Gensia Pharmaceuticals (Dr. Marangos), San Diego, CA; and Division of Restorative Neurology (Drs. He and Hsu), Baylor College of Medicine, Houston, TX.
Although hyperglycemia has been shown to consistently exacerbate ischemic brain injury following global or diffuse cerebral ischemia, the effect of hyperglycemia in unilateral focal cerebral ischemia remains controversial. Recent advances in thrombolytic therapy have enhanced the clinical significance of postischemic reperfusion. We studied the effect of plasma glucose on ischemic brain injury in a newly developed focal cerebral ischemia-reperfusion model. Rats allowed free access to food until ischemic insult developed intra-and postischemic hyperglycemia and cortical infarction. Rats fasted for 24 hours had blunted hyperglycemic responses. Infarct volumes were correspondingly smaller. The protective effect of fasting was partially abolished by glucose loading during ischemia to induce intra-ischemic hyperglycemia. Glucose loading immediately or 3 hours after focal cerebral ischemia did not significantly alter the protective effect of fasting. Insulin treatment in fed rats before ischemia also reduced hyperglycemic responses and infarct volume. Timing of insulin treatment was also critical in the reduction of ischemic injury. These findings indicate that plasma glucose during the period of ischemia is an important determinant of brain injury in focal cerebral ischemia-reperfusion and there is a therapeutic window for normalization of plasma glucose to be efficacious.
Address correspondence and reprint requests to Dr. C.Y. Hsu, Division of Restorative Neurology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030.
Supported by NIH grants NS 25545 and NS 28995.
Received September 7, 1990. Accepted for publication in final form November 28, 1990.
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