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Unanesthetized macaque monkeys were subjected to middle cerebral artery (MCA) occlusion. Local cerebral blood flow (ICBF) was measured with a hydrogen clearance technique. Mean arterial blood pressure, arterial blood gases, and intracranial pressure were monitored serially. Two weeks after ischemic insult, a neuropathologic examination documented cerebral infarction and its relation to CBF recording sites. Unanesthetized monkeys hyperventilated and became hypocapneic, particularly after MCA occlusion (mean Paco2 fell from 33 to 26 mm Hg). Intracranial pressure remained normal except in massive fatal infarction, where it rose dramatically. Responses to MCA occlusion were strikingly variable; some animals showed little ICBF reduction and no deficit or infarction, while others sustained marked ICBF reduction with hemiplegia and massive fatal infarction. Extent of ICBF reduction correlated well with infarct size. Since the extent of ICBF reduction reflects collateral circulation, variation in collateral supply appears responsible for variation of infarction. Re-opening of MCA occlusion always led to restoration of normal or above normal ICBF. Thus, no evidence for impaired reperfusion was observed. Post-ischemic CBF markedly above normal was associated with eventual severe infarction. Restoration of MCA flow led to improvement of hemiparesis after moderate reduction in ICBF, but fatal infarction occurred despite restored flow after severe reduction in ICBF. "No reflow" was not observed. When ICBF fell below 12cc/100gm/min for 2 hours or longer, local infarction resulted. Flow above this infarction threshold prevented irreversible damage.