Key result
Prolonging cerebral ischemia to 30 minutes disrupts reperfusion and causes persistent severe focal deficits.
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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.
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Ginsberg et al. (1978) studied Severe diffuse cerebral ischemia. Cerebral ischemia (15 or 30 minutes) via bilateral common carotid and basilar artery occlusion vs. Control / 15-minute vs 30-minute ischemia duration was evaluated on Local cerebral blood flow and postischemic brain perfusion. Fifteen minutes of cerebral ischemia allowed uniform recirculation at 31-35% of control flow, whereas 30 minutes caused heterogeneous perfusion with persistent severe ischemia.
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