Oxygen radical mechanisms of brain injury following ischemia and reperfusion

Oxygen radical mechanisms of brain injury following ischemia and reperfusion THE OVERALL MORTALITY and morbidity and to provide a critical assessment of the methodological limitations in delineating radical mechanisms of injury in vivo. Models of Ischemia and Reperfusion It is clear from evaluating different animal models of ischemia and reperfusion that a number of factors are important in determining the extent of neurological damage that occurs as a direct result of ischemia. These include but are not limited to the amount of blood flow reduction, the duration of time that flow is reduced, the regional location of the flow reduction, and the metabolic state of the brain before the ischemic period. Multiple mechanisms may contribute to the injury, and the relative contribution of each mechanism depends on the specific situation. For example, calcium-induced damage from the release of excitatory neurotransmitters is gen1185 Copyright 0 1991 the American Physiological Society erally most prominent with moderate reductions of blood flow in regions with high N-methyl-D-aspartate (NMDA) receptors (98) and high excitatory amino acid innervation. With severe or complete reduction of blood flow, calcium entry through non-NMDA receptor-operated channels and voltage-sensitive channels becomes prominent (127). With reduced blood flow over prolonged periods, continued anaerobic glycolysis enhances the contribution of acidosis to http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

Oxygen radical mechanisms of brain injury following ischemia and reperfusion

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Publisher
The American Physiological Society
Copyright
Copyright © 1991 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
Publisher site
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Abstract

THE OVERALL MORTALITY and morbidity and to provide a critical assessment of the methodological limitations in delineating radical mechanisms of injury in vivo. Models of Ischemia and Reperfusion It is clear from evaluating different animal models of ischemia and reperfusion that a number of factors are important in determining the extent of neurological damage that occurs as a direct result of ischemia. These include but are not limited to the amount of blood flow reduction, the duration of time that flow is reduced, the regional location of the flow reduction, and the metabolic state of the brain before the ischemic period. Multiple mechanisms may contribute to the injury, and the relative contribution of each mechanism depends on the specific situation. For example, calcium-induced damage from the release of excitatory neurotransmitters is gen1185 Copyright 0 1991 the American Physiological Society erally most prominent with moderate reductions of blood flow in regions with high N-methyl-D-aspartate (NMDA) receptors (98) and high excitatory amino acid innervation. With severe or complete reduction of blood flow, calcium entry through non-NMDA receptor-operated channels and voltage-sensitive channels becomes prominent (127). With reduced blood flow over prolonged periods, continued anaerobic glycolysis enhances the contribution of acidosis to

Journal

Journal of Applied PhysiologyThe American Physiological Society

Published: Oct 1, 1991

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