Huang, Zhihong, Ke Chen, Paul L. Huang, Seth P. Finklestein, Michael A. Moskowitz. ameliorates ischemic injury by blood flow-independent mechanisms mutant . Am. J. Physiol. 272 (Heart Circ. Physiol. 41): Hl401-H1405, 1996.-Genetically engineered deficient in the expression of type III nitric oxide synthase (NOS) [endothelial NOS (eNOS>] were used to decipher the importance of nitric oxide (NO)-dependent augmentation of regional cerebral blood flow (rCBF) to infarct volume reduction following basic fibroblast growth factor () in f us1âo n d uring acute middle cerebral artery (MCA) * occlusion. We have shown previously that intravenously administered reduces infarct volume following MCA occlusion in rats that dilates cerebral pial arterioles by NO-dependent mechanisms. Halothane-anesthetized eNOS wild-type were subjected to permanent MCA occlusion by intraluminal filament for 24 h. (100 pg. kg-l+ h-l) was infused intravenously for 2 h, beginning 15 min after the onset of occlusion. Infarct volume was reduced from 119 ? 8 to 93 t 4 mm3 (22% reduction, P < 0.05) or from 102 t 9 to 77 2 6 mm3 (24% reduction, P < 0.05) or wild-type , respectively (means t SE; n = 10 per group), neurological deficits were also significantly reduced. Although infusion caused a
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Mar 1, 1997
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