Acetylcholine attenuated norepinephrine-induced pressure responses in canine tibia by 62%, an effect abolished by inhibiting prostaglandin and EDRF synthesis (p<0.0001).
Does acetylcholine infusion modify norepinephrine-induced perfusion pressure responses in canine tibia?
Intraosseous endothelial cells can regulate long bone blood flow by secreting vasodilator prostaglandins and EDRF.
valor p: p=<0.0001
This in vitro study investigates whether intraosseous endothelial cells can regulate long bone blood flow by secretion of vasodilator prostaglandin and EDRF (endothelium-derived relaxing factor). Canine tibia were perfused through the nutrient artery at a constant flow rate, and the increases in perfusion pressure caused by standard doses of norepinephrine were recorded first under control conditions and then during acetylcholine infusion. Acetylcholine attenuated the norepinephrine pressure responses (-62 +/- 3%). This attenuating effect of acetylcholine was partially abolished by inhibition of prostaglandin synthesis (-20 +/- 6%) and completely abolished by inhibition of EDRF synthesis (+73 +/- 43%) or combined inhibition of prostaglandin and EDRF synthesis (+134 +/- 30%). These results are statistically significant (p less than 0.0001) and suggest that both EDRF and vasodilator prostaglandin are synthesized by intraosseous endothelial cells, and can modify long bone vascular resistance. Thus, as in other organs, intraosseous endothelial cells may provide bone with an autoregulatory control mechanism and enable it to respond to a diverse group of vasodilator stimuli.
Davis et al. (Fri,) reported a other. Acetylcholine infusion vs. Control conditions was evaluated on Increases in perfusion pressure caused by norepinephrine (p=<0.0001). Acetylcholine attenuated norepinephrine-induced pressure responses in canine tibia by 62%, an effect abolished by inhibiting prostaglandin and EDRF synthesis (p<0.0001).
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