Gründeman P F, Tukkie R, Moulijn A C, Rudolphy V J, de Jong J W, Frederiks W M, Gijsbers G H, Marx F, Klopper P J
Department of Experimental Surgery, Academic Medical Center, Amsterdam, The Netherlands.
Thorac Cardiovasc Surg. 1993 Oct;41(5):290-6. doi: 10.1055/s-2007-1013874.
Mechanical circulatory support is only meaningful when reversible myocardial damage exists. Prompt biventricular assistance during reperfusion for six hours was tried in the regionally sublethally injured pig myocardium which has perspective for recovery. Postmortem tissue was examined with a quickly performed histochemical technique for tissue viability. Animals underwent five coronary occlusions (5 min occlusion/10 min reperfusion). Postischemic systolic wall thickening, observed by direct echocardiography, fell about 50% (p < 0.05 vs base line) before treatment which paralleled cardiac inosine and lactate efflux. Biventricular unloading (n = 5) resulted in contractile recovery to 94 +/- 19% (p < 0.05 vs stunning), untreated pigs remained depressed (33 +/- 12%, n = 5). During circulatory support the arterial lactate levels rose three-fold, concomitant with a drop in pH of 0.2 units (p < 0.05). Post-mortem histochemistry showed scattered areas with decreased activities of cytoplasmic lactate dehydrogenase and mitochondrial beta-hydroxybutyrate dehydrogenase, irrespective of treatment. Transmission electron microscopy revealed irreversible damage to mitochondria in depleted areas in contrast to areas where enzyme activity was present. We conclude that prompt volume unloading during reperfusion accelerated contractile recovery of sublethally postischemic myocardium.
机械循环支持仅在存在可逆性心肌损伤时才有意义。在具有恢复前景的局部亚致死性损伤猪心肌中，尝试在再灌注期间进行6小时的快速双心室辅助。用一种快速的组织化学技术检查死后组织的活力。动物经历了五次冠状动脉闭塞（每次闭塞5分钟/再灌注10分钟）。通过直接超声心动图观察，缺血后收缩期室壁增厚在治疗前下降了约50%（与基线相比，p<0.05），这与心脏肌苷和乳酸流出平行。双心室卸载（n=5）导致收缩功能恢复到94±19%（与顿抑相比，p<0.05），未治疗的猪仍处于抑制状态（33±12%，n=5）。在循环支持期间，动脉乳酸水平升高了三倍，同时pH值下降了0.2个单位（p<0.05）。死后组织化学显示，无论治疗情况如何，均有散在区域的细胞质乳酸脱氢酶和线粒体β-羟基丁酸脱氢酶活性降低。透射电子显微镜显示，与存在酶活性的区域相比，耗尽区域的线粒体存在不可逆损伤。我们得出结论，再灌注期间迅速的容量卸载加速了亚致死性缺血后心肌的收缩功能恢复。
