Löwe H, Schulz U, Blasig I E
Academy of Sciences of the GDR, Institute of Drug Research.
Pharmazie. 1988 Jul;43(7):501-2.
Isolated rabbit hearts were perfused normoxically or ischemically using the technique of Langendorff. The hearts were perfused with a modified Krebs-Henseleit solution, perturbated with 95% O2/5% CO2 or in case of ischemia with N2 which replaced the O2. The perfusion rate was 25 ml/min under normoxic and 2.5 ml/min under ischemic conditions. The oxygen pressure was about 65 kPa in the normoxic and about 6 kPa in the ischemic medium. Reperfusion of ischemic hearts was realized in some cases normoxically. During the ischemic perfusion and reperfusion LDH was released time depended into the perfusion medium and the aortic inflow pressure increased. The LDH release and the increase of the inflow pressure are strong correlated. Both parameters direct to ischemic myocardial lesions. Amrinone applied as bolus in the start period of ischemia or as an infusion during the ischemic and reperfusion time limited the release of LDH and the increase of the inflow pressure. The results were discussed as a direct protecting effect of amrinone against a myocardial ischemic lesion, which is in correspondence with the improving effects of amrinone on the ischemia caused heart failure of canines in vivo, shown by Campbell et al.
采用Langendorff技术对离体兔心进行常氧或缺血灌注。心脏用改良的Krebs-Henseleit溶液灌注，在常氧条件下用95% O₂/5% CO₂混合气体通气，缺血时则用N₂取代O₂。常氧灌注速率为25 ml/min，缺血条件下为2.5 ml/min。常氧灌注液中的氧分压约为65 kPa，缺血灌注液中约为6 kPa。部分缺血心脏在常氧条件下实现再灌注。在缺血灌注和再灌注过程中，乳酸脱氢酶（LDH）随时间依赖性地释放到灌注液中，主动脉流入压升高。LDH释放与流入压升高密切相关。这两个参数均提示存在缺血性心肌损伤。在缺血起始期静脉推注氨力农，或在缺血及再灌注期间持续输注氨力农，均可限制LDH释放及流入压升高。这些结果被认为是氨力农对心肌缺血损伤具有直接保护作用，这与Campbell等人所展示的氨力农对犬体内缺血性心力衰竭的改善作用相符。
