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目的观察兔心肌缺血再灌注(I/R)损伤中内皮功能的改变以及参附注射液(SFI)对其的影响和作用机制。方法 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:①检测结扎前、缺血40min、再灌注40min三个时相点血清内皮型一氧化氮合酶(eNOS)、一氧化氮代谢产物(NOP)和血浆内皮素(ET)含量;②检测再灌注40min后心肌组织总超氧化物歧化酶(T-SOD)和丙二醛( MDA)含量;③电镜观察心肌超微结构。结果①B组与A组比较,缺血40min、再灌注40min血清eNOS、NOP明显降低,血浆ET显著增高,后两者呈显著负相关(均P<0·01) ;再灌注40min后心肌组织T-SOD明显降低,MDA明显增高(均P<0·01) ,NOP与T-SOD、ET与MDA均呈显著正相关(P<0·05) ,NOP与MDA、ET与T-SOD均呈显著负相关(P<0·05) ;心肌超微结构发生异常改变。②C组与B组比较,缺血40min、再灌注40min eNOS、NOP水平明显增高(均P<0·01) ;再灌注40min ET水平明显降低(P<0·01) ;再灌注40min后心肌组织T-SOD显著增高,MDA显著降低(均P<0·01) ;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,并能减轻心肌I/R损伤。
Objective To observe the changes of endothelial function in myocardial ischemia/reperfusion (I/R) injury in rabbits and the effect and mechanism of SFI on it. Methods Twenty-one Japanese white rabbits were randomly divided into sham-operated control group (A group), myocardial I/R model group (B group) and myocardial I/R+SFI treatment group (C group), 7 rats in each group. Detection indicators: 1 The levels of serum endothelial nitric oxide synthase (eNOS), nitric oxide metabolites (NOP), and plasma endothelin (ET) were measured before the ligation, 40 min after ischemia, and 40 min after reperfusion; 2 The contents of total superoxide dismutase (T-SOD) and malondialdehyde (MDA) in myocardial tissue were detected 40 min after reperfusion. 3 Myocardial ultrastructure was observed by electron microscopy. Results 1 Compared with group A, the serum eNOS and NOP were significantly decreased and the plasma ET was significantly increased after 40 min ischemia and 40 min reperfusion. The latter two were significantly negatively correlated (all P<0.01); and the myocardial tissue T after 40 min reperfusion. -SOD was significantly lower, MDA was significantly higher (all P<0.01), NOP was significantly positively correlated with T-SOD, ET and MDA (P<0.05), and NOP was associated with MDA, ET, and T-SOD. Significant negative correlation (P<0.05); Abnormal changes in myocardial ultrastructure. 2C group compared with group B, eNOS and NOP levels were significantly increased at 40 min and 40 min after reperfusion (all P<0.01); ET levels were significantly reduced at 40 min after reperfusion (P<0.01); myocardial tissue at 40 min after reperfusion T-SOD was significantly increased, MDA was significantly decreased (all P<0.01); abnormal changes in 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.