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目的 探讨促进或抑制一氧化氮 (NO)的合成对大鼠肝脏缺血预处理 (IPC)保护作用的影响。方法 大鼠肝脏经缺血再灌注 (I/R ,R组 )、IPC(P组 )、左旋精氨酸 (L Arg ,A组 )促进或左旋单甲基精氨酸 (L NMMA ,N组 )抑制NO合成及假手术 (C组 )后 ,观察 2、2 4h及 1周后血浆NO、天冬氨酸氨基转移酶 (AST)及丙氨酸氨基转移酶 (ALT)以及大鼠死亡率及肝脏组织病理改变。结果 A组累计死亡率低于R组及N组 (P <0 .0 5 )。A组NO水平在 2h后明显高于P组(P <0 .0 1) ;N组在 2h及 2 4h后均低于P组 (P <0 .0 5 )及A组 (P <0 .0 1) ,1周后与P组、A组及R组差异无显著性 (P >0 .0 1) ,但明显高于C组。A组及P组的血浆ALT在 2h及 2 4h后均显著低于N组 (P <0 .0 5 ) ,而N组与R组差异无显著性 (P >0 .0 5 ) ,1周后 ,A组、P组及N组间差异无显著性 ,均低于R组 (P <0 .0 5 )。结论 增加NO的产生 ,可以明显增强IPC对肝脏的保护作用 ,抑制NO合成并不能完全阻断这种保护作用 ,提示NO是IPC保护机制中的一个重要但非唯一的因素。
Objective To investigate the effects of promoting or inhibiting the protective effects of nitric oxide (NO) synthesis on rat hepatic ischemic preconditioning (IPC). Methods Rat liver was induced by ischemia / reperfusion (I / R, R group), IPC (group P), L Arg (group A), L NMMA ) Inhibited NO synthesis and sham operation (group C). The levels of NO, AST and ALT and the mortality of rats after 2, 4 and 1 week were observed And liver histopathological changes. Results The cumulative mortality in group A was lower than that in group R and group N (P <0.05). The level of NO in group A was significantly higher than that in group P after 2h (P <0.01). The level of NO in group A was significantly lower than that in group P (P <0.05) and group A at 2h and 24h (P <0. 0 1). There was no significant difference between P group, A group and R group after 1 week (P> 0.05), but it was significantly higher than that of C group. Plasma ALT in group A and group P was significantly lower than that in group N at 2 h and 24 h (P <0.05), while there was no significant difference between group N and group R (P> 0.05) There was no significant difference between group A, group P and group N, which was lower than group R (P <0.05). CONCLUSION: Increasing the production of NO significantly enhances the protective effect of IPC on the liver. Inhibition of NO synthesis does not completely block this protective effect, suggesting that NO is an important but not the only factor in IPC protection mechanism.