Influence of coronary artery obstruction on cardiac prostaglandin metabolism during experimental cardioplegic arrest.
In order to test the influence of coronary artery obstruction on cardiac prostaglandin metabolism during surgically induced cardioplegia (CP), we have measured transcardiac veno-arterial gradients of prostacyclin and thromboxane A2 (TXA A2) during experimental canine cardiopulmonary bypass. Cardiac arrest was induced by infusion of 500 ml of hypothermic (8 degrees C), hyperkalemic (25 meq) crystalloid CP solution into the aortic root with (group I) and without (group II) occlusion of the left anterior descending artery (LAD). After 30 minutes of cardioplegic arrest the LAD occlusion in group I was released and a second set of CP infusion was applied in both groups. Transcardiac gradients were obtained 5 seconds after onset of the first and second CP washouts. Significant prostacyclin and TXA A2 gradients were observed at both times. Prostacyclin gradients did not differ between group I and group II. In contrast, TXA A2 gradients were significantly higher during the second CP washout in group I as compared to the unoccluded group (group I 918 +/- 221, group II 244 +/- 144 pg/ml, p less than 0.05). The results of our study suggest that cardiac TXA A2 metabolism during cardioplegic arrest is increased distal to a coronary artery obstruction. Cardiac TXA A2 production might contribute to the increased ischemic myocardial injury observed in this setting.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood*; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000097:blood*; D002315:Cardiopulmonary Bypass; D003331:Coronary Vessels; D004285:Dogs; D005260:Female; D006324:Heart Arrest, Induced; D008297:Male; D010976:Platelet Count; D013929:Thromboxane B2 / Q000097:blood*
D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha