Endothelial control of long bone vascular resistance.
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
T R
TR
Department of Orthopaedics, Mayo Clinic and Foundation, Rochester, Minnesota 55905.
Wood
M B
MB
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001842:Bone and Bones / Q000098:blood supply* / Q000502:physiology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D008833:Microcirculation / Q000502:physiology; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D010477:Perfusion; D011453:Prostaglandins / Q000378:metabolism / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology*
D011453:Prostaglandins; D009569:Nitric Oxide; D000109:Acetylcholine; D009638:Norepinephrine