左旋精氨酸对实验性缺血/再灌注损伤心肌能量代谢的影响

目的探讨左旋精氨酸(L-Arg)对心肌缺血/再灌注损伤(MIRI)时心肌细胞能量代谢的影响及其机制。方法实验兔30只,随机分为假手术对照组(A组)、心肌缺血/再灌注组(B组)和心肌缺血/再灌注+L-Arg治疗组(C组)。在再灌注20min时,分别检测心肌组织内三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)含量,总腺苷酸量(TAN),能荷(EC),丙二醛浓度(MDA),超氧化物歧化酶(SOD)活性,一氧化氮(NO)水平及内皮素(ET)浓度,同时观察心肌超微结构的改变。结果C组与B组比较,心肌组织内ATP、ADP、TAN、NO含量,SOD活性及EC均明显增高(P<0.05,P<0.01),MDA、ET浓度均显著减少(P<0.05);与A组比较,AMP、TAN、NO、ET、MDA差异无显著性(P>0.05);心肌超微结构的异常改变显著减轻。结论L-Arg可通过降低体内氧自由基、ET水平,提高体内NO水平、SOD活性而改善缺血/再灌注损伤心肌的能量代谢。

Effect of L-arginine on myocardial cell energy metabolism during the ischemia/reperfusion injury in rabbits

Objective To study the effect of L-arginine (L-Arg) on myocardial cell energy metabolism during myocardial ischemia/reperfusion injury (MIRI) and its mechanism. Methods MIRI models of the rabbits were randomly divided into three groups (n=10, in each), cotrol group (A), MIRI group (B) and MIRI+L-Arg group (C). The contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), total adenylic acid number (TAN), energy charge (EC), nitric oxide (NO), endothelin (ET), malonyldialdehyde (MDA) and the activity of superoxide dismutase (SOD) in the myocardial tissue were measured, respectively. Meanwhile, the ultrastructure changes in myocardium were observed during MIRI. Results The ATP, ADP, TAN, EC, NO and SOD levels of myocardial tissue in C group were higher than those in B group (P<0.05 and P<0.01); the contents of ET, MDA myocardial tissue in C group were lower than those in B group (P<0.05); and there were not significant differences in ADP, AMP, TAN, NO and MDA between C and A group (P>0.05); abnormal changes of the myocardial ultrastructure in C group were ameliorated remarkably too during MIRI. Conclusions L-Arg can improve myocardial cell energy metabolism in the reperfusion injury after myocardial ischemia by decreasing oxygen free radical and ET levels, raising NO level and SOD activity.