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缺血预处理诱导的一氧化氮对大鼠肝移植冷缺血-再灌注损伤的保护作用

Protective role of nitric oxide induced by ischemic preconditioning on cold ischemic-reperfusion injury of rat liver graft.

作者信息

Xue Q, Yuan Z, Chen Z, Hao R, Liu C, Tu B

机构信息

Department of Hepatobiliary Surgery, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.

出版信息

Transplant Proc. 2012 May;44(4):948-51. doi: 10.1016/j.transproceed.2012.01.040.

DOI:10.1016/j.transproceed.2012.01.040
PMID:22564593
Abstract

AIMS

To investigate the protective role of nitric oxide (NO) induced by ischemic preconditioning (IP) on cold ischemic-reperfusion (IR) injury of rat liver grafts.

METHODS

One hundred twenty-eight male Sprague Dawley rats used for orthotopic liver transplantation were randomly divided into four groups (n = 32): administering heparin before ischemic reperfusion (control group); IP with 10-minute ischemia and 10-minute reperfusion before IR (IP group); adenosine before IR (Ade group); and L-NAME (NG-nitro-L-arginine methyl ester) + IP before IR (NAME group). Half of each group were used to investigate 1-week recipient survival rate, and another to obtain blood and hepatic tissue samples after 2-hour reperfusion.

RESULTS

One-week survival bile production, serum NO, and antioxidase activity were higher but serum alanine aminotransferase, tumor necrosis factor-α, and superoxide levels in hepatic tissue were lower in the IP group and Ade group versus the control group or NAME group. Liver sinusoidal endothelial cells in the IP and Ade groups showed less injury than the other groups.

CONCLUSION

NO induced by IP can improve 1-week survival and rat liver function as well as protect liver sinusoidal endothelial cells.

摘要

目的

研究缺血预处理(IP)诱导的一氧化氮(NO)对大鼠肝移植冷缺血再灌注(IR)损伤的保护作用。

方法

将128只用于原位肝移植的雄性Sprague Dawley大鼠随机分为四组(n = 32):缺血再灌注前给予肝素(对照组);IR前进行10分钟缺血和10分钟再灌注的IP处理(IP组);IR前给予腺苷(Ade组);以及IR前给予L-NAME(NG-硝基-L-精氨酸甲酯)+ IP(NAME组)。每组一半用于研究1周受体存活率,另一半用于在再灌注2小时后获取血液和肝组织样本。

结果

与对照组或NAME组相比,IP组和Ade组的1周存活率、胆汁生成、血清NO和抗氧化酶活性较高,但血清丙氨酸转氨酶、肿瘤坏死因子-α和肝组织中的超氧化物水平较低。IP组和Ade组的肝窦内皮细胞损伤比其他组少。

结论

IP诱导的NO可提高大鼠1周存活率和肝功能,并保护肝窦内皮细胞。

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Aggravation of post-ischemic liver injury by overexpression of insulin-like growth factor binding protein 3.
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