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目的观察实验兔心肌缺血再灌注(I/R)损伤中内皮功能的改变和参附注射液(SFI)对它的影响及作用机制。方法把21只日本大耳白兔随机分为假手术对照组(A组)、心肌I/R模型组(B组)及心肌I/R+SFI治疗组(C组),每组7只。检测指标:结扎前、缺血40min、再灌注40min3个时相点血清一氧化氮代谢产物(NOP)和血浆内皮素(ET)的含量;再灌注40min后心肌组织总超氧化物歧化酶(T-SOD)和丙二醛(MDA)的含量;电镜观察心肌的超微结构。结果B组与A组比较,缺血40min、再灌注40min血清NOP明显降低,血浆ET显著增高,且二者呈显著负相关;再灌注40min后心肌组织T-SOD明显降低,MDA明显增高,NOP与T-SOD、ET与MDA均呈显著正相关,NOP与MDA、ET与T-SOD均呈显著负相关;心肌的超微结构发生异常改变。C组与B组比较,缺血40min、再灌注40minNOP水平明显增高;再灌注40minET水平明显降低;再灌注40min后心肌组织T-SOD显著增高,MDA显著降低;心肌超微结构的异常改变明显减轻。结论SFI具有改善兔心肌I/R中自由基介导的内皮功能紊乱作用,可减轻心肌的I/R损伤。
Objective To observe the changes of endothelial function in myocardial ischemia/reperfusion (I/R) injury in experimental rabbits and the effect and mechanism of Shenfu injection (SFI) on it. The method of 21 Japanese white rabbits were randomly divided into sham operation group (A), myocardial I / R model group (group B) and myocardial I / R + SFI group (group C), n = 7. Detection index: Serum nitric oxide metabolites (NOP) and plasma endothelin (ET) content before ligating, 40 min ischemia, and 40 min reperfusion; total myocardial superoxide dismutase (T) after 40 min reperfusion -SOD) and malondialdehyde (MDA) content; Electron microscopic examination of the ultrastructure of the myocardium. Results Compared with group A, serum NOP was significantly decreased and plasma ET was significantly increased in group B and group A after 40 min of ischemic reperfusion. There was a significant negative correlation between the two groups. After 40 min of reperfusion, the T-SOD of myocardium significantly decreased and MDA significantly increased. There was a significant positive correlation between T-SOD, ET and MDA. There was a significant negative correlation between NOP and MDA, ET and T-SOD. The abnormal ultrastructure of myocardium was changed. Compared with group B, the levels of NOP at 40 minutes after ischemia and 40 minutes after reperfusion increased significantly, and the level of ET at 40 minutes after reperfusion decreased significantly. After 40 minutes of reperfusion, the T-SOD in the myocardial tissue significantly increased and the MDA significantly decreased; the abnormal changes of myocardial ultrastructure were significantly reduced. . Conclusion SFI can improve the function of free radical-mediated endothelial dysfunction in rabbit myocardial I/R and reduce myocardial I/R injury.