SUMMARY Glucose was Infused intravenously into cats prior to cerebral ischemia. Brain concentrations of glucose, measured in 7 regions, were elevated 2.5-fold compared to those of non-infused animals. Ischemia of 15 or 30 minutes duration caused a greater accumulation of lactic add in the brain of glucose-infused animals. Post-iscbemic restitution of cerebral ATP, phospbocreatine, and lactate during 90 minutes of reclrculation was severely impaired in the brain of animals pretreated with glucose compared to untreated animals. Thus, excess lactic addosis may be a major factor interfering with metabolic restitution following cerebral ischemia. Stroke, Vol 11, No 4, 1980CEREBRAL ISCHEMIA causes rapid depletion of the brain's stores of high energy phosphates -ATP and phosphocreatine. 1 "' Recirculation following defined periods of ischemia leads, in many models, to nearly complete recovery of brain levels of ATP and phosphocreatine.1 "* Recently, however, we have described regionally heterogeneous recovery of brain blood flow and metabolite levels following 30 minutes, but not 15 minutes, of ischemia in the cat. '8 Thus, a 90-minute recirculation period following a 30-minute ischemic insult produced regions in which ATP and phosphocreatine levels were less than 10% of control."In the present study we have examined the effect of pre-ischemic administration of glucose on restitution of metabolite levels following 15 or 30 minutes of ischemia. Glucose administration has previously been shown to increase the neurologic deficit and degree of neuropathologic damage caused by cardiac arrest in the monkey. "11 Since post-ischemic recovery of brain function depends upon restoration of an adequate energy state, we have compared restitution of energy metabolites in glucose-treated versus untreated animals which have been described previously. 1 In the accompanying report 18 we have examined the effect of glucose infusion on post-ischemic cerebral blood flow. MethodsCats of either sex, weighing 3-4 kg, were anesthetized with sodium pentobarbital, 40 mg/kg intraperitoneally, and were prepared as previously described.1 ' The common carotid arteries were isolated and encircled with loose-fitting ligatures, and the basilar artery was exposed through the clivus. One

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The effects of severe cerebral ischemia on postischemic brain perfusion were examined in a series of pentobarbital-anesthetized cats. Ischemia of 15 or 30 minutes' duration was produced by occlusion of both common carotid arteries and the basilar artery and was coupled with mild systemic hypotension. A 90-minute period of normotensive postischemic recirculation was permitted in some animals. In 9 of 10 animals studied at the end of the ischemic insult and not allowed to recover, blood flow in the cerebral hemispheres was greatly reduced, with minimal flow (0.01 to 0.11 ml gm-1 min-1) persisting only in scattered perisulcal regions in 4 animals. Following 15 minutes of ischemia, blood flow was restored uniformly during recirculation, though at subnormal levels (31 to 35% of control). In contrast, 30 minutes of prior ischemia led to marked heterogeneities of local cerebral perfusion during recirculation, with multiple zones of persistent severe ischemia. Thus, while recirculation was suboptimal following both 15 and 30 minutes of ischemia, the 30-minute insult led to focal postischemic perfusion abnormalities that were sufficiently severe to make the possibility of functional recovery appear unlikely.