Irikura K, Huang P L, Ma J, Lee W S, Dalkara T, Fishman M C, Dawson T M, Snyder S H, Moskowitz M A
Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA.
Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):6823-7. doi: 10.1073/pnas.92.15.6823.
Nitric oxide (NO) is known to mediate increases in regional cerebral blood flow elicited by CO2 inhalation. In mice with deletion of the gene for neuronal NO synthase (NOS), CO2 inhalation augments cerebral blood flow to the same extent as in wild-type mice. However, unlike wild-type mice, the increased flow in mutants is not blocked by the NOS inhibition, N omega-nitro-L-arginine, and CO2 exposure fails to increase brain levels of cGMP. Topical acetylcholine elicits vasodilation in the mutants which is blocked by N omega-nitro-L-arginine, indicating normal functioning of endothelial NOS. Moreover, immunohistochemical staining for endothelial NOS is normal in the mutants. Thus, following loss of neuronal NOS, the cerebral circulatory response is maintained by a compensatory system not involving NO.
已知一氧化氮（NO）可介导吸入二氧化碳引起的局部脑血流量增加。在神经元型一氧化氮合酶（NOS）基因缺失的小鼠中，吸入二氧化碳后脑部血流量增加的程度与野生型小鼠相同。然而，与野生型小鼠不同的是，突变体中血流量的增加并未被NOS抑制剂Nω-硝基-L-精氨酸阻断，且暴露于二氧化碳未能增加脑部cGMP水平。局部应用乙酰胆碱可使突变体血管舒张，该作用可被Nω-硝基-L-精氨酸阻断，表明内皮型NOS功能正常。此外，突变体内皮型NOS的免疫组织化学染色也正常。因此，在神经元型NOS缺失后，脑循环反应由一个不涉及NO的代偿系统维持。
