RESUMO
Twelve anesthetized open chest dogs received an intracoronary infusion of 20 muCi of 3H-arachidonic acid through the left anterior descending coronary artery. A control blood sample was then taken from the great cardiac vein. The left anterior descending coronary artery was occluded for 10 minutes and then released. A second cardiac vein blood sample was obtained during the coronary reactive hyperemic response. The pre-and postocclusion blood samples were analyzed for prostaglandin (PG)-like substances using thin-layer chromatography and analysis for radioactivity. There was an increase in PGE2- and PGA2-like substances, and arachidonic acid found in the postocclusion samples. PGE2 appears to be the predominant prostaglandin formed. Three animals received 10 mg/kg of indomethacin intravenously 1 hour before the 3H-arachidonic acid infusion. Pretreatment with indomethacin abolished the release of PGE2 and PGA2-like substances but no arachidonic acid and reduced the reactive hyperemic response in magnitude and duration. Reactive hyperemia after a 10-minute occlusion was studied in five dogs before and 1 hour after the intravenous administration of 10 mg/kg of indomethacin. The control coronary flow and peak reactive hyperemic response were significantly reduced by the indomethacin. These studies suggest that myocardial ischemia promotes the synthesis and release of PG-like substances which may play a role in reactive hyperemia.
