Does of the local myocardial release of prostaglandin E2 or F2α contribute to the early consequences of acute myocardial ischaemia?

The possible role of prostaglandins in acute myocardial ischaemia was investigated in anaesthetized greyhounds which were subjected to either short (3 min) occlusions or permanent ligation of the left anterior descending coronary artery. Plasma PGE₂ and PGF_2α concentrations were measured by radioimmunoassay in blood from the aorta, the coronary sinus (draining the essentially normal myocardium) and from a local coronaryvein (draining the area rendered ischaemic by coronary artery ligation). In the permanent ligation studies PGE₂ and PGF_2α were measured before, and 2, 10 and 30 min post-ligation. At 2 and 10 min post ligation there were no significant changes in the concentrations of either prostaglandin in blood from the essentially normal myocardium or from the acutely ischaemic myocardium. After 30 min of coronary artery ligation there was a significant increase in PGE₂ in the local coronary vein. This release of PGE₂ from the ischaemic myocardium was not related to the occurrence of cardiac dysrhythmias but may reflect the onset of changes in cellular integrity in the developing area of infarction. Despite electrocardiographic and metabolic evidence of acute myocardial ischaemia there was no increase in PGE₂ or PGF_2α values in either the coronary sinus or the local coronary vein following the release of a 3-min coronary artery occlusion. Since neither PGE₂ nor PGF_2α is released from the acutely ischaemic myocardium during the first 10 min post-ligation or during reperfusion following 3-min occlusions, it is unlikely that either of these prostaglandins is involved in the early consequence of coronary artery ligation.