中文摘要：

目的研究内源性一氧化碳对大鼠离体心脏心肌缺血再灌注损伤的影响。方法大鼠经内源性一氧化碳激动药物原卟啉氯化钴（CoPP）处理后，采用Langendorff离体心脏灌流系统制作心肌缺血再灌注实验模型，采集记录离体心脏稳定期和缺血30min再灌注时的左室收缩终末压（LVESP）、左心室舒张终末压（LVEDP）、心率（HR）、左室发展压（LVDP）、左室最大收缩速率（＋dP／dtmax）和左室最大舒张速率（-dP／dtmax）等心功能指标，探讨内源性一氧化碳对大鼠心肌缺血再灌注损伤的影响。结果在停灌前稳定期，对照组和药物组心脏各项指标均保持平稳。两组间指标无显著性差异；停灌30min后复灌，对照组较未停灌前心功能各项指标明显下降，且变化较大，对心脏的舒缩功能影响较大，该组比停灌前LVESP下降了19．8％，＋dP／dtmax下降了28．5％，-dP／dtmax的绝对值下降了33．6％，差异均具有显著性（P〈0．05）。而药物组复灌后各项心功能指标变化较小，仍保持着停灌前的平稳水平，对心脏的舒缩功能影响较小，且复灌后达到稳定所用的时间较对照组明显缩短（P〈0．05）。结论内源性一氧化碳对正常情况下心室的舒缩功能影响不大，但对心肌缺血再灌注损伤具有一定的保护作用。

英文摘要：

Objective To explore the effect endogenous carbon monoxide on myocardial ischemia reperfusion injuryafter Cobalt Protoporphyrin（CoPP） treatment.Method The rats were treated with CoPP（ Agonist of endogenous carbon monoxide）.The myocardial ischemia reperfusion model was established by Langendorff isolated cardiac per- fusion system.The 1 eft ventricular systolicpressure （LVESP）, left ventricular end-diastolic pressure （LVEDP）, left ventricular developed pressure（ LVDP ）, the maximum rate of left ventricular pressure （ ＋dP/dtmax ） were obtained. Result Before reperfusion, all parameters remained stable in control group and CoPP group, and no significant difference between the two groups. After reperfusion, the control group＇ s cardiac function decreased significantly （P〈0.05） ,the LVESP decreased 19%, ＋dP/dtmax, decreased 28.5% and -dP/dtmax decreased 33.6%.Comparedwith the control group, the CoPP group＇ s cardiac function did not change significantly, while still maintaining a rel- atively stable level. Conclusion The endogenous carbon monoxide has no effect on normal cardiac function, but it has positive effect on the cardiac abnormaldiastolic and systolic function, that protect the cardiac function from myo- cardial ischemia reperfusion injury.