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Project Title:
The role of 20 Hete in the Pathogenesis of Stroke
Funding Agency:
NIH
Total Project Period:
Apr 1, 2005 – Mar 31, 2006
Principal Investigator:
Patrick Kochanek, MD (Dr. Horowitz, MD, Principal Investigator)
Project Summary:
Decreasing tissue infarction in the ischemic penumbra is the primary therapeutic target after stroke. The degree of tissue damage in the ischemic penumbra is a function of the severity of the ischemic insult, which is partially regulated y the cerebral microvascular resistance. Recent studies have shown that the monohydroxylated metabolite of arachidonic acid, 10-hydroxyeicosatetraenoic acid (20-HETE) is an important regulator of cerebrovascular resistance and is an important regulator of the vasoactive effects of nitric oxide.
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