外源性一氧化碳抗大鼠肢体缺血再灌注所致心肌损伤的实验研究

Effect of exogenous carbon monoxide on myocardial damage induced by ischemia reperfusion in rats

目的外源性一氧化碳对大鼠肢体由缺血再灌注(IR)导致心肌损伤的治疗及机制。方法 22只大鼠随机分为IR组(10只)、IR吸入CO组(RC组)(10只)、假手术组(S组)(2只);检查大鼠心肌组织及横纹变化,肌组织中Bax、Bcl-2及凋亡百分比,肌酸激酶同工酶(CK-MB)和血清乳酸脱氢酶(LDH)水平。结果 RC组大鼠肌组织中Bcl-2水平明显高于IR组(P<0.05),而其余指标则均显著低于IR组(P<0.05),心肌损伤相对减轻。结论外源性CO可减轻肢体IR导致的心肌损伤,其可能与抑制中性粒细胞在肌组织内聚集有关。

Objective To investigate the protective effect of exogenous carbon monoxide（ CO） on myocardium damage induced by ischemia-reperfusion（ IR） in right hind limb of rats,and to explore its action mechanism. Methods Twenty-two Sprague-Dawley rats were randomly divided into three groups： IR group（ n = 10）,IR ＋ CO group（ n = 10） and sham-operation group（ n = 2）. The changes of myocardial structure and transverse striation were observed,and the apoptosis rate,expression levels of Bax and Bcl-2 in myocardial tissues,the activities of lactate dehydrogenase（ LDH） and creatine kinase isoenzyme（ CK-MB） in serum were detected. Results The expression levels of Bcl-2 in IR ＋ CO group were significantly higher than those in IR group,however,the other indexes in IR ＋ CO group were obviously lower than those in IR group,with milder myocardial damage in IR ＋ CO group. Conclusion The exogenous carbon monoxide can mitigate myocardial damage induced by ischemia reperfusion in rats,its action mechanism may be related with suppressing neutrophil aggregation in myocardial tissue.