CONTRIBUTION OF PROSTAGLANDINS TO EXERCISE-INDUCED VASODILATION IN HUMANS

It has been postulated that endothelial release of prostaglandins cont ributes to exercise-induced vasodilation of skeletal muscle arterioles . To test this hypothesis, 12 normal subjects underwent brachial arter ial and venous catheter insertion and instrumentation of their forearm to measure plethysmographic forearm blood flow. Forearm blood flow an d arterial and venous 6-ketoprostaglandin F1alpha (PGF1alpha) and pros taglandin E2 (PGE2) were then measured during two levels of wrist flex ion exercise (0.2 and 0.4 W). In nine of the subjects, exercise was re peated after intra-arterial infusion of indomethacin (0.3 mg/100 ml fo rearm vol). Exercise increased forearm blood flow (2.0 +/- 0.2 to 12.1 +/- 1.1 ml.min-1.100 ml-1) and forearm release of PGF1alpha (162 +/- 28 to 766 +/- 193 pg.min-1 . 100 ml-1) and PGE2 (26 +/- 6 to 125 +/- 4 6 pg.min-1.100 ml-1) (all P < 0.05). Indomethacin virtually abolished forearm prostaglandin release and reduced forearm blood flow at rest ( 2.2 +/- 0.2 to 1.7 +/- 0.2 ml.min-1 . 100 ml-1), at 0.2 W (6.3 +/- 0.7 to 5.4 +/- 0.7 ml.min-1.100 ml-1), and at 0.4 W (12.2 +/- 1.5 to 10.3 +/- 1.3 ml.min-1.100 ml-1) (all P < 0.02). These data suggest that re lease of vasodilatory prostaglandins contributes to exercise-induced a rteriolar vasodilation and hyperemia in skeletal muscle.