一氧化氮在急性肝衰竭实验模型中的肝保护作用。
Hepatoprotective effect of nitric oxide in experimental model of acute hepatic failure.
作者信息
Saracyn Marek, Brytan Marek, Zdanowski Robert, Ząbkowski Tomasz, Dyrla Przemysław, Patera Janusz, Wojtuń Stanisław, Kozłowski Wojciech, Wańkowicz Zofia
机构信息
Marek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
出版信息
World J Gastroenterol. 2014 Dec 14;20(46):17407-15. doi: 10.3748/wjg.v20.i46.17407.
AIM
To evaluate the effect of nitric oxide (NO) on the development and degree of liver failure in an animal model of acute hepatic failure (AHF).
METHODS
An experimental rat model of galactosamine-induced AHF was used. An inhibitor of NO synthase, nitroarginine methyl ester, or an NO donor, arginine, were administered at various doses prior to or after the induction of AHF.
RESULTS
All tested groups developed AHF. Following inhibition of the endogenous NO pathway, most liver parameters improved, regardless of the inhibitor dose before the induction of liver damage, and depending on the inhibitor dose after liver damage. Prophylactic administration of the inhibitor was more effective in improving liver function parameters than administration of the inhibitor after liver damage. An attempt to activate the endogenous NO pathway prior to the induction of liver damage did not change the observed liver function parameters. Stimulation of the endogenous NO pathway after liver damage, regardless of the NO donor dose used, improved most liver function parameters.
CONCLUSION
The endogenous NO pathway plays an important role in the development of experimental galactosamine-induced AHF.
目的
在急性肝衰竭（AHF）动物模型中评估一氧化氮（NO）对肝衰竭发展及程度的影响。
方法
采用半乳糖胺诱导的AHF实验大鼠模型。在诱导AHF之前或之后，以不同剂量给予NO合酶抑制剂硝基精氨酸甲酯或NO供体精氨酸。
结果
所有测试组均发生了AHF。抑制内源性NO途径后，大多数肝脏参数得到改善，这与肝损伤诱导前抑制剂的剂量无关，而取决于肝损伤后的抑制剂剂量。预防性给予抑制剂在改善肝功能参数方面比肝损伤后给予抑制剂更有效。在诱导肝损伤之前激活内源性NO途径的尝试并未改变观察到的肝功能参数。肝损伤后刺激内源性NO途径，无论使用的NO供体剂量如何，大多数肝功能参数均得到改善。
结论
内源性NO途径在实验性半乳糖胺诱导的AHF发展中起重要作用。
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