Durante W, Schafer A I
Department of Medicine, Houston VA Medical Center, TX, USA.
Int J Mol Med. 1998 Sep;2(3):255-62. doi: 10.3892/ijmm.2.3.255.
Carbon monoxide (CO) is an endogenously generated gas that may play an important physiological role in the circulation. CO is generated by vascular cells as a byproduct of heme catabolism, in which heme oxygenase (HO) catalyzes the degradation of heme to biliverdin, iron and CO. Two distinct isoforms of HO have been identified in vascular tissue. The HO-2 isoform is constitutively expressed and likely mediates the release of CO under normal physiologic conditions. In contrast, the HO-1 isoform is strongly induced in vascular cells by various stress-associated agents and markedly increases CO synthesis during pathological conditions. The release of CO by vascular cells exerts both paracrine and autocrine effects on vascular smooth muscle cells (SMC) and circulating blood cells. CO regulates blood flow and blood fluidity by inhibiting vasomotor tone, SMC proliferation, and platelet aggregation. These vascular effects of CO are mediated via the activation of soluble guanylate cyclase and the consequent rise in intracellular guanosine 3',5'-cyclic monophosphate levels in target tissues. CO may also play a role in various cardiovascular disorders, including endotoxin shock, ischemia-reperfusion, hypertension, and subarachnoid hemorrhage. This review will focus on the recent progress made in understanding the regulation and function of CO in the vasculature.
一氧化碳（CO）是一种内源性生成的气体，可能在循环系统中发挥重要的生理作用。CO由血管细胞作为血红素分解代谢的副产物生成，其中血红素加氧酶（HO）催化血红素降解为胆绿素、铁和CO。在血管组织中已鉴定出两种不同的HO同工型。HO-2同工型组成性表达，可能在正常生理条件下介导CO的释放。相反，HO-1同工型在血管细胞中被各种应激相关因子强烈诱导，在病理条件下显著增加CO的合成。血管细胞释放的CO对血管平滑肌细胞（SMC）和循环血细胞发挥旁分泌和自分泌作用。CO通过抑制血管运动张力、SMC增殖和血小板聚集来调节血流和血液流动性。CO的这些血管效应是通过可溶性鸟苷酸环化酶的激活以及靶组织中细胞内鸟苷3',5'-环磷酸水平的相应升高来介导的。CO还可能在各种心血管疾病中起作用，包括内毒素休克、缺血再灌注、高血压和蛛网膜下腔出血。本综述将聚焦于在理解CO在血管系统中的调节和功能方面取得的最新进展。
