Nowicki P T, Miller C E
Department of Pediatrics, Ohio State University, Columbus 433205, USA.
Pediatr Res. 1995 Nov;38(5):783-91. doi: 10.1203/00006450-199511000-00024.
The goal of these experiments was to determine the presence and mechanistic basis of flow-induced dilation in mesenteric artery from 3-d-old swine. In the first experiment, in vitro gut loops were perfused from a blood-filled reservoir under controlled-flow conditions, and flow was progressively increased from approximately 40% to approximately 170% in six increments by manipulation of pump speed. Under control conditions, vascular resistance significantly decreased after each step increase in flow rate. NG-Monomethyl-L-arginine (LNMMA; 10(-4) M), an arginine analog that blocks nitric oxide production, eliminated this flow-induced dilation, but only for the step increases in flow at rates above the baseline flow rate. For step increases below the baseline rate, LNMMA caused a simple parallel shift of the resistance-flow rate curve upward. Phenylephrine (10(-6) M), an alpha 1-agonist which has no effect on nitric oxide production or half-life, did not eliminate flow-induced dilation, but instead caused a simple parallel shift of the resistance-flow rate curve upward across the entire range of flows studied. In the second experiment, a 3-cm segment of mesenteric artery was perfused with Krebs buffer at two flow rates: 10 and 25 mL/min. The effluent from the mesenteric artery segment was suffused onto a deendothelialized, phenylephrine-precontracted ring of swine carotid artery; relaxation of this bioassay vessel served as an index of release of relaxing factors from the mesenteric artery segment. Under control conditions, increase in the mesenteric artery flow rate caused a 60% relaxation of the bioassay vessel. This effect was eliminated by the addition of LNMMA to the buffer (10(-4) M), but not by the addition of indomethacin (10(-5) M). Flow-induced dilation occurs in the mesenteric artery of 3-d-old swine. This vascular phenomenon appears to be mediated by nitric oxide, but only at flows above the baseline flow rate. The mechanism(s) responsible for this phenomenon at lower flow rates is not clear.
