INFLUENCE OF VENULAR PROSTAGLANDIN RELEASE ON ARTERIOLAR DIAMETER DURING FUNCTIONAL HYPEREMIA

Indomethacin treatment or removal of the venular endothelium will atte nuate functional arteriolar vasodilation in the hamster cremaster musc le. We tested the hypothesis that prostanoid release from venular endo thelial cells was responsible for the functional vasodilation of the p aired arteriole. The hamster cremaster muscle was prepared for in vivo microscopy and stimulated for 1 minute (10V, 40 mu sec, 1 Hz). Before a second muscle stimulation, the venular endothelium was removed by p erfusing the venule with several air bubbles. A third muscle stimulati on was performed during prostaglandin inhibition (28 mu mol/L indometh acin superfusion). Arterioles (n=9, 55+/-5 mu m) dilated 25+/-4% durin g the initial muscle stimulation. After removal of the endothelium fro m the paired venules, there was no effect on resting arteriolar diamet ers (53+/-4 mu m), but the functional arteriolar dilation was attenuat ed to 15+/-5% (P<.05). The additional indomethacin treatment had a sig nificant effect on resting diameter (50+/-4 mu m) but did not alter th e magnitude of the functional vasodilation (11+/-4%, P>.05). In a seco nd set of experiments, the order of the experimental protocol was reve rsed. Muscle stimulation resulted in a 23+/-2% increase in diameter (4 7+/-2 to 57+/-2 mu m). Indomethacin treatment significantly attenuated the functional dilation to 8+/-3% (45+/-2 to 48+/-2 mu m). Arteriolar diameter was significantly smaller after disruption of the venular en dothelium with air bubbles (40+/-2 mu m), but there was no effect on t he functional vasodilation, 8+/-3% increase in diameter (to 43+/-2 mu m). These results suggest that the arteriolar dilatory response to mus cle stimulation is mediated, in part, by prostanoid release from the v enular endothelium.