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Oxygen radicals in cerebral ischemia
C W Nelson1, E P Wei, J T Povlishock
1Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
The American Journal of Physiology
|November 1, 1992
Summary
Superoxide production during reperfusion after cerebral ischemia damages blood vessels and increases blood-brain barrier permeability. Antioxidant treatment with superoxide dismutase (SOD) and catalase mitigates these harmful effects.
Area of Science:
- Neuroscience
- Biochemistry
- Physiology
Background:
- Cerebral ischemia-reperfusion injury involves complex pathophysiological processes.
- Superoxide radical production is implicated in post-ischemic vascular dysfunction and blood-brain barrier (BBB) breakdown.
Purpose of the Study:
- To investigate the role of superoxide production in cerebral ischemia-reperfusion injury.
- To determine the contribution of superoxide to vascular abnormalities and BBB permeability.
- To explore the potential therapeutic effects of antioxidants.
Main Methods:
- Measurement of superoxide production using nitro blue tetrazolium (NBT) reduction in cats subjected to cerebral ischemia-reperfusion.
- Assessment of vascular responses to hypocapnia and acetylcholine.
- Evaluation of blood-brain barrier permeability using labeled albumin and horseradish peroxidase.
- Administration of superoxide dismutase (SOD) plus catalase and deferoxamine as pretreatment.
Main Results:
- Significant superoxide production was detected during the early reperfusion period, lasting over an hour.
- Ischemia-reperfusion reduced vasoconstrictor responses to hypocapnia and altered acetylcholine responses, effects prevented by SOD/catalase or deferoxamine.
- Blood-brain barrier permeability increased post-ischemia, an effect minimized by SOD and catalase pretreatment.
- The normal vasodilator response to acetylcholine was preserved with SOD and catalase treatment.
Conclusions:
- Superoxide generation persists for a significant duration during reperfusion following cerebral ischemia.
- Superoxide and its derivatives contribute to post-ischemic vasodilation, abnormal vascular reactivity, and increased BBB permeability.
- Hydroxyl radical, generated via the iron-catalyzed Haber-Weiss reaction, is suggested as the primary mediator of vascular abnormalities.