论文部分内容阅读
目的 :研究一氧化氮 /内皮素 - 1(NO/ET - 1)失衡与肝缺血再灌注 (I/R)损伤的关系以及肝缺血预处理 (IPC)对NO/ET - 1系统的调节作用。方法 :采用鼠肝I/R模型 ,比较I/R组和IPC +I/R组NO/ET - 1系统的变化情况及其与肝I/R损伤的关系。用RT -PCR检测再灌注 2h内肝组织中是否有诱生性一氧化氮合酶(iNOS)mRNA表达。结果 :再灌注急性期血浆NO代谢产物 (NO-2 /NO-3 )降低、ET - 1升高致NO/ET - 1比值降低 ,血浆ALT、AST、LDH、TNF -α含量及肝组织丙二醛 (MDA)含量增高 ,而肝组织ATP含量降低 ,肝损伤加重 ;肝IPC的保护作用与其升高NO-2 /NO-3 、降低ET - 1,升高NO/ET - 1比值有关 ;在上述肝组织中未测出有iNOSmR NA表达。结论 :肝I/R损伤与NO/ET - 1失衡有关 ,IPC对I/R急性期肝的保护作用可能是通过对NO/ET - 1系统的调节作用而介导的 ,此时NO来源于原生性一氧化氮合酶 (cNOS)而非iNOS
AIM: To investigate the relationship between the imbalance of nitric oxide / endothelin - 1 (NO / ET - 1) and hepatic ischemia / reperfusion (I / R) injury and the effect of hepatic ischemic preconditioning (IPC) Regulatory effect. Methods: The changes of NO / ET - 1 system in I / R group and IPC + I / R group were compared with the I / R model of rat liver to determine the relationship between I / R injury and hepatic I / R injury. The expression of inducible nitric oxide synthase (iNOS) mRNA in liver tissue was detected by RT-PCR 2h after reperfusion. Results: In the acute phase of reperfusion, the levels of plasma NO metabolites (NO-2 / NO-3) and ET-1 increased, the ratio of NO / ET-1 decreased and the levels of plasma ALT, AST, LDH and TNF- The content of MDA increased, while the content of ATP in liver tissue decreased and the liver injury increased. The protective effect of IPC on liver was related to the increase of NO-2 / NO-3, ET-1 and NO / ET-1. No iNOSmR NA expression was detected in the above liver tissues. Conclusions: I / R injury in the liver is related to the imbalance of NO / ET - 1. The protective effect of IPC on acute liver injury in I / R may be mediated through the regulation of NO / ET - 1 system. Native nitric oxide synthase (cNOS) but not iNOS