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Diffuse cerebral ischemia in the cat: I. Local blood flow during severe ischemia and recirculation

Diffuse cerebral ischemia in the cat: I. Local blood flow during severe ischemia and recirculation 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

Diffuse cerebral ischemia in the cat: I. Local blood flow during severe ischemia and recirculation

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References (60)

Publisher
Wiley
Copyright
Copyright © 1978 the American Neurological Association
ISSN
0364-5134
eISSN
1531-8249
DOI
10.1002/ana.410030605
pmid
677814
Publisher site
See Article on Publisher Site

Abstract

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.

Journal

Annals of Neurology – Wiley

Published: Jun 1, 1978

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