| Objectives:By studying the changes in levels of nitric oxide (NO), endothelin (ET-1) and circulating endothelial cells (CEC), and that in functions of coronary vasomotor, the author discusses the protective effects of adenosine-Lidocaine cardioplegia on endothelial cells of Canine coronary vascular and its possible mechanism. Methods:This study is divided into two parts; the first part to establish dog open heart surgery under cardiopulmonary bypass model to simulated clinical cardiac operation. Through the dog’s vital signs and hemodynamic indexes clarify dog extracorporeal circulation operation of anaesthesia management features. In the second part 12 mongrel dogs were randomly divided into Adenosine lidocaine cardioplegia (Adenosine-lidocaine cardioplegia, AL group, n=6) and the ST. Thomas Ⅱ cardioplegia group (K group, n=6). Measured the changes in levels of NO, ET-1 and CEC on three time points:before operation (T1),1h afterheart re-beating(T2) and 2h after heart re-beating(T3), observed the changes in functions of coronary vasodilation, and analyzed the ultrastructure by using transmission electron microscope. Results:The preoperative data of the two groups has no significant differences. On the time point of T3, NO in plasma of group K has been significantly decreased than that of group AL (P<0.05). ET-1 has been increased significantly (P<0.05), so as CEC(P<0.05). The maximum percentage of coronary vasodilation in group K is 29.13%±8.24% which is lower than that of AL group 68.52%±11.32%(P<0.01). Electron microscopy results show that the damage of coronary vascular endothelial cell ultrastructure of group K is more serious than that of group AL. Conclusion:The protective effect of adenosine-Lidocaine cardioplegia on canine coronary vascular endothelial cell is superior to that of ST.Thomas Ⅱ cardioplegia. |
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