Adenovirus-mediated heme oxygenase-1 gene transfection prevents hemoglobin-induced contraction of rat basilar artery.
Adenovirus-mediated heme oxygenase-1 gene transfection prevents hemoglobin-induced contraction of rat basilar artery.
复制标题
腺病毒介导的血红素加氧酶-1基因转染可防止血红蛋白诱导的大鼠基底动脉收缩。
DOI：
10.1007/978-3-7091-6232-3_20
复制
发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Macdonald,RL
中科院分区：
文献类型：
--
作者：
Ono,S;Komuro,T;Macdonald,RL
血管痉挛是蛛网膜下腔红细胞溶解的结果，释放血红蛋白和可能的其他致痉挛物质。SAH后早期清除血凝块，无论是手术还是脑池内纤溶组织纤溶酶原激活剂或尿激酶，都可以预防血管痉挛[1]。鉴于血红蛋白在血管痉挛发病机制中的关键作用，血红蛋白和血红素代谢的改变可能对预防血管痉挛很重要。氧合血红蛋白或脱氧血红蛋白中的亚铁氧化产生高铁血红蛋白，高铁血红蛋白更容易从球蛋白链中释放出血红素基团。珠蛋白链可能被细胞内和细胞外蛋白酶降解。血红素组通过血红素加氧酶（HO）代谢为胆绿素、一氧化碳（CO）和铁，血红素加氧酶由至少3种同工酶组成，包括氧化应激诱导蛋白HO-1 [2]。
Vasospasm is a consequence of erythrocyte lysis in the subarachnoid space that releases hemoglobin and possibly other spasmogenic substances. Removing the blood clot early after SAH, either surgically or by intracisternal fibrinolysis with tissue plasminogen activator or urokinase, may prevent vasospasm [1]. In view of the critical role that hemoglobin appears to play in the pathogenesis of vasospasm, modification of the metabolism of hemoglobin and heme may be im- portant to preventing vasospasm. Oxidation of ferrous iron in oxy- or deoxyhemoglobin produces meth- emoglobin that more readily releases its heme groups from the globin chains. Globin chains probably are degraded by intra- and extracellular proteases. The heme group is metabolized to biliverdin, carbon mon- oxide (CO) and iron by heme oxygenases (HO) that consist of at least 3 isozymes including the oxidative stress-inducible protein HO-1 [2].