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作 者:詹勇强[1] 吕新生[1] 王志明[1] 李宜雄[1] 胡国璜[1] 曾庆华[1]
出 处:《中华实验外科杂志》2002年第4期338-339,共2页Chinese Journal of Experimental Surgery
摘 要: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 study the effect of nitiric oxide (NO) on the protection of ischemic precondition (IPC) of rat liver.Methods Rats were assigned to 5 groups: group R (ischemia/reperfusion,I/R),group P (IPC),group A (L Arg+IPC+I/R),group N (L NMMA+IPC+I/R) and group C (Pseudo operation).The serum NO level,activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST),rat mortality and liver histopathology were investigated 2?h,24?h and 1 week after operation.Results The total mortality was significantly lower in group A than in group R and group N (P<0.05,both).NO level in group A after 2?h was significantly higher than in group P (P< 0.01) ; but significantly lower after 2 and 24?h in group N (P<0.05,both).1 week later,no significant difference showed between these 3 groups.ALT levels in group A and group P were significantly lower than in group N (P<0.05,all).1 week later,no significant differences show between these 3 groups. Conclusion Inducing the NO producing can effectively enhance the protection of liver from I/R injury,but inhibiting it cannot block this protective effect completely.It suggests that NO play an important,but not the only role in the rat liver IPC.
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