Deleterious effect of glucose pretreatment on recovery from diffuse cerebral ischemia in the cat. I. Local cerebral blood flow and glucose utilization.

TLDR: Diffuse cerebral ischemia was created in pentobarbital-anesthetized cats by basllar and bilateral carotid artery occlusions and hypotension, and deoxyglucose autoradiograms in the latter animals were remarkable for a complete suppression of tracer uptake in the cerebral cortex and a paradoxically increased tracer concentration inThe cerebral white matter.

Abstract: Diffuse cerebral ischemia was created in pentobarbital-anesthetized cats by basilar and bilateral carotid artery occlusions and hypotension. Local cerebral blood flow (ICBF) was assessed autoradiographically with 14C-antipyrine, and local cerebral glucose utilization with 14C-2-deoxyglucose. In animals without glucose pretreatment, 15 min of ischemia led to a homogeneous reduction of post-ischemic cerebral perfusion to 31% of control; ischemia of 30 min produced post-ischemic perfusion heterogeneities in the cerebral cortex and deep gray structures. In animals pretreated with dextrose, 1.5 gm/kg intravenously, heterogeneous cerebral perfusion was observed following only 15 min of ischemia, and a severe global impairment of cerebral reperfusion occurred after the 30 min insult. Deoxyglucose autoradiograms in the latter animals were remarkable for a complete suppression of tracer uptake in the cerebral cortex and a paradoxically increased tracer concentration in the cerebral white matter. Mean plasma glucose in the treated animals exceeded 1000 mg/100 ml. Large glucose loads prior to ischemia dramatically impair post-ischemic cerebral perfusion.