实验性缺血再灌注心肌顿抑与一氧化氮的关系及东莨菪碱对其影响

Relationship between myocardial stunning and nitric oxide (NO) after experimental ischemia/reperfusion and the beneficial effect of scopolamine

目的探讨体外循环缺血再灌注心肌顿抑与心肌一氧化氮（ＮＯ）产生之间的关系及东莨菪碱对其影响。方法１２只绵羊，随机均分为：对照组和实验组：即东莨菪碱治疗组。常规建立体外循环，对照组主动脉阻断同时灌注冷停搏液（本院配方）；实验组，停搏液中加入东莨菪碱１７．５μｇ／ｋｇ。于主动脉阻断前、再灌注５分钟、再灌注３０分钟取冠状窦血检测ＮＯ、肌酸激酶（ＣＫ）、环磷酸鸟苷（ｃＧＭＰ）浓度，取心肌测定丙二醛（ＭＤＡ）含量，相应时点监测心功能。结果再灌注５分钟和３０分钟时，对照组心肌血的ＮＯ、ＣＫ、ｃＧＭＰ、ＭＤＡ均明显升高，与主动脉阻断前相比差异有显著性（Ｐ＜０．０５或＜０．００１），和实验组相同时间点相比差异有显著性（Ｐ＜０．０５或＜０．０１）。两组再灌注５分钟和３０分钟时心肌功能均降低，对照组较实验组更为显著。再灌注后ＮＯ的变化与心肌ＭＤＡ和ＣＫ之间呈正相关（Ｐ＜０．０５和０．０１）。结论缺血再灌注心肌顿抑与ＮＯ产生增加有关，大量释放的ＮＯ提高心肌组织ｃＧＭＰ，参与心肌细胞脂质过氧化损害心肌功能。东莨菪碱减少ＮＯ产生、保护顿抑心肌的作用可能与其抗脂质过氧化有关。

Objective Studies on alterations of the production of myocardial nitric oxide (NO) during ischemia/reperfusion were carried out. The relationship between myocardial stunning and NO was observed on 12 sheep divided randomly into two groups: control (Ⅰ, n=6) and scopolamine treated (Ⅱ, n=6). Methods Cardiopulmonary bypass (CPB) was instituted routinely and cold cardioplegic solution was administered into the root of aorta. In group I, Renji solution was infused and in group Ⅱ scopolamine (17.5 μg/kg) was added into Renji solution. Blood samples were taken from coronary sinus before aortic crossclamping (A), 5 min(B) and 30 min (C) after reperfusion. Parameters including NO, CK, cGMP were measured. Specimens of myocardium were taken for MDA content assay and cardiac performance was measured at the corresponding time points. Results Concentrations of NO, CK, cGMP and myocardial MDA content increased significantly in group I at time B and C, as compared with time A ( P <0.05—0.001) and the same time points in group Ⅱ ( P <0.05—0.01). Parameters of cardiac funciton were found to be decreased in both groups but more significant decrease was found in group I than in group Ⅱ. There was positive correlation between the changes of NO and myocardial MDA content or CK ( P <0.005 and P <0.01, respectively) after reperfusion. Conclusion The excessive production of NO during reperfusion may contribute to myocardial stunning. The marked increase of NO was deleterious to cardiac function by increasing myocardial cGMP and peroxidizing the myocyte membrane lipid. The beneficial influence of scopolamine by reducing the production of NO and improving the function of stunned myocardium was related to its effects of preventing myocardial cell lipid peroxidation.