含血停跳液对缺氧未成熟心肌的保护作用

The experimental study of myocardial protection using blood cardioplegia for hypoxic immature myocardium

目的 探讨含血停跳液对缺氧未成熟心肌的保护作用。方法 构建缺氧幼兔模型 ,观察应用含血停跳液灌注 (研究组 )与冷晶体停跳液灌注 (对照组 )后幼兔心肌收缩力、冠脉流量 ,心肌含水量和心肌细胞超微结构的变化。结果 复跳后心肌收缩力的恢复率分别为 :研究组 ( 97 5 0± 4 11) % ,对照组 ( 5 6 2 5± 9 48) % (P <0 0 1) ;缺血期不同时点 ( 0 ,2 0 ,40min)的冠脉流量分别为 :研究组 3 5 3± 0 3 2 ,3 45± 0 44 ,3 4± 0 5ml/(min·g) ,对照组 2 0 9± 0 2 6,1 86±0 3 ,1 79± 0 2ml/(min·g) (P <0 0 1) ;复跳后不同时点 ( 0 ,10 ,2 0min)的冠脉流量分别为 :研究组 3 5 9± 0 3 2 ,3 7± 0 2 9,3 88± 0 3 7ml/(min·g) ,对照组 2 96± 0 2 5 ,2 74± 0 2 8,2 3 5± 0 2 6ml/(min·g) (P <0 0 1) ;再灌注末心肌含水量 :研究组 ( 5 9 95± 2 0 9) % ,对照组 ( 79 77± 1 17) % ,(P <0 0 1)。研究组心肌细胞线粒体、细胞核等超微结构得到较好保护。结论 应用含血停跳液灌注后的冠脉流量 ,复跳后心肌收缩力的恢复率较高 ;缺血后心肌水肿较轻 。

Objective To explore the myocardial protection using the blood cardioplegia for hypoxic immature myocardium. Methods A hypoxic model of neonatal rabbits was established in this study. Indexes including the recovery of myocardial contractility (%)(MCR), the coronary sinus flow (CSF), water content and myocardial ultrastructure were observed after warm induction and reperfusion with blood cardioplegia, and were compared to cold crystalloid cardioplegia. Results\ MCR was (97 50±4 11)% in study group versus (56 25±9 48)% in control group( P <0 01); CSF in ischemia at the times of 0, 20, 40 minutes was 3 53±0 32 ,3 45±0 44 and 3 4±0 5 ml/(min·g)in study group versus 2 09±0 26,1 86±0 3 and 1 79±0 2 ml/(min·g)in control group respectively( P <0 01);CSF after reperfusion at the times of 0,10 20 minutes was 3 59±0 32,3 7±0 29 and 3 88±0 37 ml/(min·g)in study group versu 2 96±0 25,2 74±0 28 and 2 35±0 26 ml/(min·g)in control group respectively ( P <0 01); Myocardial water content was (59 95±2 09) % in study group versus (79 77±1 17) % in control group ( P <0 01). The myocardial ultrastructure was protected by warm induction and reperfusion with blood cardioplegia. Conclusion\ Warm induction and reperfusion with blood cardioplegia can improve the CSF both in ischemia and after reperfusion. There are better myocardial contractility and myocardial protection of cell ultrastructure after myocardial reperfusion with blood cardioplegia.