Mechanism of reperfusion arrhythmia prostaglandin as a washout metabolite.

This study was designed to clarify the mechanism of reperfusion arrhythmia. In the mongrel dogs, the left anterior descending coronary artery was occluded for 15 min and then the ligation was released. The dogs were divided into two groups: one was the control group, and the other the indomethacin group in which indomethacin, an inhibitor of prostaglandin (PG) biosynthesis, was premedicated at 30 min before ligation. The ventricular multiple response threshold (VMRT), and plasma levels of K+, PG E and PG F2 alpha were measured in the great cardiac vein before and during occlusion, and after reperfusion. In the control group, during occlusion, VMRT decreased and did not return to normal soon after reperfusion. The levels of PG E and PG F2 alpha in the great cardiac vein did not change significantly during occlusion; however, PG E became significantly elevated after reperfusion. In the indomethacin group, the time course of VMRT was essentially similar to that of the control group during occlusion; however, lowering of VMRT after reperfusion was prevented significantly. The PG F2 alpha level in the great cardiac vein did not elevate after reperfusion or during occlusion. In both groups, the level of K+ in the great cardiac vein was elevated during occlusion, but rapidly decreased to normal after reperfusion. These results suggest that PG E, as a washout metabolite, is a key factor in evoking reperfusion arrhythmia.