Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm

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 inhibitorN^G-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 ml^{1 ·} 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 ^· min^{1 ·} 100 mlforearm^{1 ·} 100 mmHg of perfusionpressure^{1 ·} min¹,P < 0.05; FBF = 26.6 ± 2.9 vs.22.8 ± 2.6 ml ^· 100 ml^{1 ·} 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 ml^{1 ·} 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.