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肝脏缺血/再灌注会诱发大鼠心脏损伤。

Ischemia/reperfusion of the liver induces heart injury in rats.

作者信息

Chen C F, Wang D, Lin H I, Leu F J, Shen C Y, Chou C-C

机构信息

Department of Internal Medicine, Cheng Hsin General Hospital, Taipei, Taiwan, Republic of China.

出版信息

Transplant Proc. 2007 May;39(4):855-7. doi: 10.1016/j.transproceed.2007.02.041.

Abstract

OBJECTIVE

We evaluated the cardiovascular injury induced by ischemia and reperfusion (I/R) of the liver by measuring changes in blood levels of cardiac troponin I (cTNI), an index of cardiovascular injury, as well as levels of selected indicators of an inflammatory response.

MATERIALS AND METHODS

Ischemia was induced in the rat liver by clamping the common hepatic artery and portal vein for 40 minutes, after which flow was restored, and the liver reperfused for 90 minutes. Blood samples were collected prior to ischemia and after reperfusion. cTNI as well as levels of tumor necrosis factor alpha (TNFalpha), hydroxyl radical (.OH), nitric oxide (NO), and alanine transferase (ALT) were measured.

RESULTS

I/R of the liver induced a significant increase in ALT (P<.001). Increased cTNI levels (P<.05) were associated with inflammatory responses, such as elevated levels of TNFalpha (P<.001), . OH (P<.001), and NO (P<.001). After administration of 3-aminobenzamide, a poly(ADP-ribose) polymerase (PARP) inhibitor, liver and heart injuries were significantly attenuated (P<.05).

CONCLUSIONS

I/R-induced liver injury was associated with cardiovascular injury, perhaps resulting from inflammatory responses triggered by elevated levels of reactive radical species of nitric oxide, superoxide, and peroxynitrite, by which PARP was activated. 3-Aminobenzamide, significantly attenuated I/R-induced liver and heart injuries.

摘要

目的

通过测量心血管损伤指标心肌肌钙蛋白I(cTNI)的血液水平变化以及炎症反应相关指标的水平,评估肝脏缺血再灌注(I/R)诱导的心血管损伤。

材料与方法

通过夹闭大鼠肝总动脉和门静脉40分钟诱导肝脏缺血,之后恢复血流,肝脏再灌注90分钟。在缺血前和再灌注后采集血样。检测cTNI以及肿瘤坏死因子α(TNFα)、羟自由基(·OH)、一氧化氮(NO)和丙氨酸转氨酶(ALT)的水平。

结果

肝脏I/R导致ALT显著升高(P<0.001)。cTNI水平升高(P<0.05)与炎症反应相关,如TNFα(P<0.001)、·OH(P<0.001)和NO(P<0.001)水平升高。给予聚(ADP-核糖)聚合酶(PARP)抑制剂3-氨基苯甲酰胺后,肝脏和心脏损伤明显减轻(P<0.05)。

结论

I/R诱导的肝脏损伤与心血管损伤相关,可能是由一氧化氮、超氧阴离子和过氧亚硝酸盐等活性自由基水平升高引发的炎症反应所致,PARP由此被激活。3-氨基苯甲酰胺显著减轻了I/R诱导的肝脏和心脏损伤。

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