Soluble Guanylate Cyclase α1β1 Limits Stroke Size and Attenuates Neurological Injury

摘要

Background and PurposeNitric oxide (NO) mediates endothelium-dependent vasodilation, modulates cerebral blood flow (CBF), and determines stroke outcome. NO signals in part by stimulating soluble guanylate cyclase (sGC) to synthesize cGMP. To study the role of sGC in stroke injury, we compared the outcome of cerebral ischemia and reperfusion in mice deficient in the α1 subunit of sGC (sGCα1^−/−) to that on wild-type (WT) mice.