Prostaglandins and exercise hyperemia of dog skeletal muscle.
The possibility that prostaglandins (PG) contribute to skeletal muscle exercise hyperemia was tested by blocking PG synthesis with indomethacin and by measuring muscle prostaglandin E (PGE) release. The anterior calf muscles of anesthetized dogs were stimulated at frequencies of 1 Hz, 3 Hz, and 6 Hz under conditions of free flow both before and after indomethacin (5 mg/kg). PGE release was elevated from 14.2 +/- 2.4 to 21.8 +/- 3.4 ng . min-1 . 100 g-1 (P less than 0.01) during stimulation at 3 Hz and from 17.5 +/- 5.1 to 39.2 +/- 9.8 ng . min-1 . 100 g-1 (P less than 0.05) during stimulation of 6 Hz. During exercise at 1 Hz, PGE release was not increased. Indomethacin blocked PGE release and the vascular response to arachidonic acid, but caused essentially no changes in blood flow, oxygen consumption, and vascular conductance during exercise at each frequency. Thus, although PGE release is increased during free flow exercise, inhibiting PG synthesis does not alter exercise hyperemia. However, resting vascular conductance is significantly decreased by indomethacin.
D000818:Animals; D004285:Dogs; D007213:Indomethacin / Q000494:pharmacology; D009132:Muscles / Q000098:blood supply* / Q000378:metabolism / Q000502:physiology; D010101:Oxygen Consumption; D005082:Physical Exertion; D011458:Prostaglandins E / Q000378:metabolism*; D011863:Radioimmunoassay; D012039:Regional Blood Flow
D011458:Prostaglandins E; D007213:Indomethacin