Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm |
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Authors: | Engelke, Keith A. Halliwill, John R. Proctor, David N. Dietz, Niki M. Joyner, Michael J. |
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Abstract: | Engelke, Keith A., John R. Halliwill, David N. Proctor, NikiM. Dietz, and Michael J. Joyner. Contribution of nitric oxide andprostaglandins to reactive hyperemia in the human forearm. J. Appl. Physiol. 81(4):1807-1814, 1996.We investigated the separate and combinedcontributions of nitric oxide (NO) and vasodilating prostaglandins asmediators of reactive hyperemia in the human forearm. Forearm bloodflow (FBF) was measured with venous occlusion plethysmography after 5 min of ischemia. In one protocol (n = 12), measurements were made before and after intra-arterialadministration of the NO synthase inhibitorNG-monomethyl-L-arginine(L-NMMA) to one forearm. In aseparate protocol (n = 7),measurements were made before and after systemic administration of thecyclooxygenase inhibitor ibuprofen and again afterL-NMMA.L-NMMA reduced baseline FBF atrest (2.7 ± 0.4 to 1.6 ± 0.2 ml · 100 ml1 · min1;P < 0.05) and had a modesteffect on peak forearm vascular conductance and flow (forearm vascularconductance = 31.1 ± 3.1 vs. 25.7 ± 2.5 ml · min1 · 100 mlforearm1 · 100 mmHg of perfusionpressure1 · min1,P < 0.05; FBF = 26.6 ± 2.9 vs.22.8 ± 2.6 ml · 100 ml1 · min1,P = 0.055). Total excessflow above baseline during reactive hyperemia was unaffected byL-NMMA (14.3 ± 3.0 vs. 13.1 ± 2.3 ml/100 ml; P < 0.05).Ibuprofen did not change FBF at rest, reduced peak FBF from 27.6 ± 1.9 to 20.3 ± 2.7 ml · 100 ml1 · min1(P < 0.05), but had no effect ontotal excess flow above baseline. Infusion ofL-NMMA after ibuprofen reducedFBF at rest by 40%, had no effect on peak flow, but reduced totalexcess flow above baseline from 12.0 ± 2.5 to 7.6 ± 1.3 ml/100ml (P < 0.05). These datademonstrate that NO synthase inhibition has a modest effect on peakvasodilation during reactive hyperemia but plays a minimal role later.Prostaglandins appear to be important determinants of peak flow. Theeffects of NO synthase inhibition during reactive hyperemia may also bepotentiated by concurrent cyclooxygenase inhibition. |
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