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.