Mochizuki S, Okumura M, Tanaka F, Sato T, Kagami A, Tada N, Nagano M
Department of Medicine, Aoto Hospital, Jikei University School of Medicine, Tokyo, Japan.
Cardiovasc Drugs Ther. 1991 Mar;5 Suppl 2:269-76. doi: 10.1007/BF00054748.
The effect of high- and low-density lipoproteins separated from human serum on the postischemic reperfusion arrhythmias was investigated. The hearts were perfused by working heart mode with Krebs Henseleit bicarbonate buffer containing arachidonic acid (1 microgram/ml) for 5 minutes. Whole heart ischemia was induced by the use of a one-way ball valve, and hearts were perfused for 15 minutes followed by 20 minutes of reperfusion. Physiologic concentrations of high- and low-density lipoproteins were constantly infused through the atrial route during ischemic perfusion. Coronary effluent was collected via pulmonary artery cannulation for subsequent radioimmunoassay of thromboxane B2 and 6-keto-prostaglandin F1 alpha, the major stable metabolites of thromboxane A2 and prostacyclin, respectively. The incidence of ventricular arrhythmias during reperfusion was 6/6 (100%), 1/6 (17%), and 6/6 (100%) in control, high-density lipoprotein and low-density lipoprotein infusion groups, respectively. There was no significant difference in coronary flow among the three groups throughout the perfusion. Both thromboxane B2 and 6-keto-prostaglandin F1 alpha increased significantly during ischemia compared with preischemic values in all groups of hearts. However, the ratio of these two parameters varied in control and low-density lipoprotein infusion groups during ischemia, while there was no significant change in the high-density lipoprotein infusion group. These results provide the possibility that arachidonate metabolites may be involved in the regulation of ischemia-reperfusion arrhythmias and that high-density lipoprotein that was infused during ischemia markedly inhibits the incidence of ischemia-reperfusion-induced ventricular arrhythmias, due in part at least, to stabilizing the arachidonate metabolites during ischemic perfusion.
研究了从人血清中分离出的高密度脂蛋白和低密度脂蛋白对缺血后再灌注心律失常的影响。采用工作心脏模式，用含花生四烯酸（1微克/毫升）的Krebs Henseleit碳酸氢盐缓冲液灌注心脏5分钟。使用单向球阀诱导全心缺血，心脏灌注15分钟，随后再灌注20分钟。在缺血灌注期间，通过心房途径持续输注生理浓度的高密度脂蛋白和低密度脂蛋白。通过肺动脉插管收集冠状动脉流出液，用于随后对血栓素B2和6-酮-前列腺素F1α进行放射免疫测定，它们分别是血栓素A2和前列环素的主要稳定代谢产物。再灌注期间，对照组、高密度脂蛋白输注组和低密度脂蛋白输注组室性心律失常的发生率分别为6/6（100%）、1/6（17%）和6/6（100%）。在整个灌注过程中，三组之间的冠状动脉血流量没有显著差异。与所有心脏组缺血前的值相比，缺血期间血栓素B2和6-酮-前列腺素F1α均显著增加。然而，在缺血期间，对照组和低密度脂蛋白输注组这两个参数的比值有所变化，而高密度脂蛋白输注组则没有显著变化。这些结果提示，花生四烯酸代谢产物可能参与缺血-再灌注心律失常的调节，并且缺血期间输注的高密度脂蛋白可显著抑制缺血-再灌注诱导的室性心律失常的发生率，至少部分原因是在缺血灌注期间稳定了花生四烯酸代谢产物。
