Article date: February 2004
By: Victor Dishy, Paul A. Harris, Rosanna Pierce, Harish C. Prasad, Gbenga Sofowora, Holly L. Bonar, Alastair J. J. Wood, C. Michael Stein, in Volume 57, Issue 2, pages 209-212
Aims To examine the hypothesis that sildenafil, a phosphodiesterase type 5 inhibitor that inhibits cGMP breakdown, could enhance nitric oxide‐mediated vasodilation and reverse endothelial dysfunction in chronic smokers.
Methods Flow‐mediated dilation of the brachial artery and forearm postischemic reactive hyperemia (both nitric oxide‐mediated responses) were measured before and after sildenafil 50 mg and placebo in a double‐blind, randomized, crossover study in 9 men who were chronic smokers (21 ± 3 pack years).
Results There was no significant change in flow‐mediated dilation after either sildenafil (0.18%, 95%CI −1.7–2%) or placebo (0.24%, 95%CI −2.8–3.3%) (P = 0.88 and 0.8, respectively). Sildenafil had no significant effect on resting forearm blood flow or postischemic reactive hyperemia (P = 0.39 and 0.7, respectively). Resting heart rate and blood pressure were unaffected by sildenafil.
Conclusions Acute sildenafil administration did not improve endothelial function in chronic smoking men.
DOI: 10.1046/j.1365-2125.2003.01974.x
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