Dissimilar Effects of Prostacyclin, Prostaglandin E1, and Prostaglandin E2 on Myocardial Infarct Size after Coronary Occlusion in Conscious Dogs

• Published in: Circulation research 1981-09, Vol.49 (3), p.685-700
• Main Authors: JUGDUTT, BODH I, HUTCHINS, GROVER M, BULKLEY, BERNADINE H, BECKER, LEWIS C
• Format: Article
• Language: English
• Subjects: Animals; Arterial Occlusive Diseases - complications; Arterial Occlusive Diseases - mortality; Coronary Vessels - physiopathology; Dogs; Electrocardiography; Epoprostenol - pharmacology; Hemodynamics; Myocardial Infarction - complications; Myocardial Infarction - pathology; Myocardial Infarction - physiopathology; Prostaglandins - pharmacology; Prostaglandins E - pharmacology; Regional Blood Flow; Ventricular Fibrillation - complications
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.49.3.685

We studied the effects of prortaglandin 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 (0.6 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 weighed 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 PGIi and PGE2 compared to PGE1, 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 8th 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 PGʼs 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.