Boyd, L.M., Division of Cardiology, Department of Medicine, Neurobiology Research Unit, Bethesda, MD 20814, United States, Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Neurobiology Research Unit, Bethesda, MD 20814, United States
Ezra, D., Division of Cardiology, Department of Medicine, Neurobiology Research Unit, Bethesda, MD 20814, United States, Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Neurobiology Research Unit, Bethesda, MD 20814, United States
Feuerstein, G., Division of Cardiology, Department of Medicine, Neurobiology Research Unit, Bethesda, MD 20814, United States, Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Neurobiology Research Unit, Bethesda, MD 20814, United States
Goldstein, R.E., Division of Cardiology, Department of Medicine, Neurobiology Research Unit, Bethesda, MD 20814, United States, Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Neurobiology Research Unit, Bethesda, MD 20814, United States

Intracoronary leukotriene D4, 0.1-3.0 μg (0.2-6.0 nmol), produced dose-dependent decreases in coronary flow of anesthetized pigs. Pretreatment with intracoronary FPL-55712 (0.1, 0.3 and 1.0 mg) reduced coronary constriction due to 1.0 μg leukotriene D4 by up to 77%. FPL-55712 did not produce sustained alterations is coronary flow, left ventricular end-diastolic pressure, systemic arterial pressure, or heart rate. Indomethacin pretreatment (6 mg/kg i.v.) had no effect on leukotriene-induced coronary constriction. Inhibition produced by FPL-55712 may be useful in disease states involving leukotriene-mediated coronary constriction. © 1983.