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Forearm reactive hyperaemia is not mediated by nitric oxide in healthy volunteers
Author(s) -
Ailish G. Nugent,
C. McGurk,
Daniel F. McAuley,
S. Maguire,
Bernard Silke,
G D Johnston
Publication year - 1999
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1046/j.1365-2125.1999.00032.x
Subject(s) - hyperaemia , forearm , brachial artery , medicine , omega n methylarginine , reactive hyperemia , nitric oxide , blood flow , vasodilation , anesthesia , plethysmograph , cardiology , blood pressure , surgery , nitric oxide synthase
Aims To determine the role of nitric oxide (NO) in forearm reactive hyperaemia in healthy human subjects.Methods Ten healthy subjects aged 19–34 years underwent brachial artery cannulation. Forearm circulatory arrest was achieved by means of an upper arm cuff inflated to 200 mmHg for 5 min. The blood flow responses during reactive hyperaemia were measured using venous occlusion plethysmography following a 10 min intra‐arterial influsion of 8 μmol min −1 N‐monomethyl l‐arginine (‐NMMA) and following matching placebo administered in random order. Results were analysed by repeated measures anova and t ‐tests.Results ‐NMMA resulted in a significant reduction of basal forearm blood flow indicating inhibition of basal NO release (P=0.005). There was no significant difference between the blood flow responses during reactive hyperaemia following ‐NMMA and placebo (P =0.97).Conclusions Nitric oxide production does not make a significant contribution to the vasodilatation associated with reactive hyperaemia in the human forearm.