Improvement for myocardial preservation using extracorporeal shock wave

体外冲击波随种子在超声波作用下的水中穿过体内组织，在体外可促进血管生成。ESW还被证明能改善局部心肌血流量和心功能。本研究的目的是评估(1)体外冲击波能否改善心肌再灌注损伤，以及(2)是否能缩小接受体外冲击波治疗的兔心脏的心肌梗死范围。第一种实验方案为心脏停搏后切取接受体外震波治疗3d的心脏，然后在UW液中4℃保存6h。采用跨循环系统进行再灌流。再灌注1h后，在工作模式准备状态下测量左房压力(LAP)为6 mm Hg时的主动脉流量(AOF)。起搏速度为250次/分钟，主动脉后负荷压固定为60毫米汞柱。体外冲击波治疗组(L组)和非治疗组(C组)在6 mm HgLAP时的AOF分别为125±10.7ml/min和102±24.4m1/min。体外冲击波治疗有改善心肌功能的趋势。血清肌酸激酶同工酶(CK-MB)在60min时L组为5.0±0.8 ng/min，C组为13.6±4.6 ng/ml。120min时，L组CK-MB为6.6±1.3 ng/ml，C组为23.4±9.4 ng/ml。第二种方案是结扎接受ESW治疗3d的左前降支，测量心肌梗死危险面积比率(%AAR)。L组和C组的AAR分别为42%和46%。L组与C组比较差异无统计学意义。

Extracorporeal shock wave (SW) travels with the seed in water of ultrasound through body tissue, and could enhance angiogenesis in vitro. ESW has also been demonstrated to improve the local myocardial blood flow and cardiac function. The purpose of this study is to assess (1) whether ESW improves myocardial reperfusion injury, and (2) reduces the myocardial infarct size in the rabbit heart that received ESW therapy. The experimental protocol in the first was that the heart received ESW therapy for 3 days was harvested after cardioplegic arrest,and then stored in UW solution for 6 hours in 4℃. Reperfusion was performed using cross-circulation system. One hour after reperfusion, the aortic flow rate (AoF) was measured at left atrial pressure ( LAP) of 6mmHg in the working mode preparation. The heat rate was paced at 250/min, and the aortic afterload pressure was fixed at 60mmHg. The AoF at LAP of 6mmHg was 125±10.7ml/min in ESW therapy group ( L group) and 102 ±24.4m1/min in non-therapy group ( C group). ESW therapy has the tendency to improve myocardial function. Serum creatine kinase-MB ( CK-MB) on 60minute was 5.0±0.8ng/min in L group and 13.6±4.6ng/ml in C group, respectively. CK-MB on 120minute was 6.6±1.3ng/ml in L group and 23.4±9.4ng/ml in C group, respectively. The protocol in the second was that the left anterior descending artery of the heart received ESW therapy for 3 days was ligated, and we measured the rate of myocardial infarct area at risk (%AAR). The %AAR in L and C groups was 42% and 46%, respectively. There was no statistical difference between L and C groups.