Assessment of Endothelial Function in the Radial Artery Using Inhaled Albuterol

Endothelial dysfunction is an early indicator of developing atherosclerosis and is a strong predictor of future heart attack and stroke. At present, evaluation of endothelial function (EF) (specifically, EF mediated by nitric oxide, NO) is too technically difficult to form part of a routine clinical examination. Non-invasive methods that measure NO- dependent EF in arteries make use of a 4-5 minute blood pressure cuff occlusion of the arm in order to induce reactive hyperemia (RH) upon cuff release. The increased blood flow that results from the RH stimulates the endothelial cells to release NO and relax the surrounding vascular smooth muscle. The magnitude of the change in arterial caliber or stiffness provides a measure of EF. The cuff occlusion is uncomfortable and inflation and release inevitably move the arm, increasing the technical difficulty of obtaining reliable measurements. In addition, the measured endothelial response is dependent on the degree of RH, which is influenced by many confounding physiological mechanisms. Studies have shown that the beta₂-adrengergic agonist albuterol induces NO-mediated vasorelaxation in resistance vessels of humans. We examine, for the first time, the effect of albuterol on conduit vessels (radial artery) by measuring changes in the transit times of artificial pulses observed after inhalation of albuterol. We conclude that albuterol is able to relax the radial artery and that this correlates with the effects of RH (r=0.62, p=0.04). However, the response to a dose of 360 mug is smaller and more variable when compared to the response to RH-based stimulus.