Dissimilar effects of prostacyclin, prostaglandin E₁, and prostaglandin E₂ on myocardial infarct size after coronary occlusion in conscious dogs

We studied the effects of prostaglandin PGE₁, PGE₂, and prostacyclin (PGI₂) on collateral blood flow (CBF) and myocardial infarct size in conscious dogs. Beginning 5 minutes after acute permanent occlusion of the mid left circumflex coronary artery, 6-hour infusions of PGE₁ (0.5 μg/kg per min in 150 saline, 13 dogs), PGE₂ (0.7 μg/kg per min in 150 ml saline, 11 dogs), PGI₂ (0.5 μg/kg per min in 150 saline, 19 dogs) or saline alone (150 ml, 15 control dogs) were given into the left atrium. In the three treatment groups, similar reductions occurred in mean arterial pressure (PGE₁, 11%, PGE₂, 10%; PGI₂, 5%) and mean left atrial pressure (PGE₁, 44%; PGE₂, 30%; PGI₂, 36%), whereas heart rate was unchanged. Mean arterial pressure remained above 80 mm Hg throughout the infusions. After the dogs were killed 2 days later, the boundaries of the occluded bed were defined by coronary arteriography. The mass of infarct and occluded bed were measured by planimetry of weighted transverse sections of the left ventricle (LV). Although the mass of occluded bed and LV were similar in the four groups, infarct size was significantly less (P<0.005) with PGI₂ and PGE₁ compared to PGE₂ or controls, both as percent LV (4.7 vs. 7.3 vs. 14.4 vs. 14.8%, respectively) and as percent of the occluded bed (12.3 vs. 16.4 vs. 38.5 vs. 37.7%, respectively). Over the 6-hour infusion period, CBF (7-10 μm radioactive microspheres) increased throughout the occluded bed in PGI₂ and PGE₁ but not in PGE₂ and control dogs. Transmural CBF (ml/min per g) by the 6th hour, in the center of the infarct region, was greater (P<0.05) in PGI₂ (0.30 ± 0.05) and PGE₁ (0.28 ± 0.04) than in PGE₂ (0.09 ± 0.03) or control dogs (0.11 ± 0.01). Since peripheral hemodynamic effects with the different PG's were similar, myocardial protection with PGI₂ and PGE₁ appears to be attributable largely to the increase in collateral flow. However, both PGI₂ and PGE₁ also produced myocardial salvage in hearts with low levels of collateral flow, suggesting that cellular and metabolic effects may also have contributed to their protective action.