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Journal of Applied Physiology, Vol 78, Issue 2 478-482, Copyright © 1995 by American Physiological Society
ARTICLES |
I. Shrier and S. Magder
Herzl Family Practice Centre, Sir Mortimer B. Davis Jewish General Hospital, Montreal, Quebec, Canada.
Hindlimb pressure-flow relationships are well characterized by modeling a vascular waterfall at the arteriolar level. Under these conditions, Q = (Pper - Pcrit)/Rart, where Q is blood flow, Pper is perfusion pressure, Pcrit is waterfall pressure, and Rart is the resistance upstream from the waterfall. To determine the effects of endothelium-derived relaxing factor (EDRF) on Pcrit, Rart, and venous resistance (Rv), we varied Pper in the canine hindlimb between 100 and 200 mmHg before and after NG-nitro-L-arginine infusion (L-NNA, an inhibitor of EDRF synthesis). Before L-NNA, Pcrit increased with increasing Pper. After L-NNA, Pcrit was higher at each Pper, and the increase in Pcrit with increases in Pper was greater than under control conditions. In contrast to Pcrit, Rart decreased with increasing Pper before L-NNA. After L-NNA, Rart was higher at each Pper and no longer decreased with increasing Pper. Rv was not affected by Pper under control conditions but decreased with increasing Pper after L-NNA. The pressure in the small venules at each Pper decreased after L-NNA. In a second group of animals, we infused phenylephrine to control for increased tone produced by L-NNA. Results were similar to those seen with L-NNA. In conclusion, blocking EDRF synthesis increases both Pcrit and Rart, but the same response was also obtained with phenylephrine.
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