Carbon monoxide induces relaxation of human internal thoracic and radial arterial grafts.

Carbon monoxide is produced by the degradation of heme by intracellular heme-oxygenase. The aim of our study was to evaluate, in vitro, the vasodilating effect of carbon monoxide and its mechanisms of action on human internal thoracic and radial artery grafts. Segments of human internal thoracic artery and radial artery, obtained from isolated coronary artery bypass surgery patients, were studied in organ chambers. The arterial rings were precontracted with norepinephrine then submitted to carbon monoxide. Inhibitors of nitric oxide synthase and of soluble guanylate cyclase were added to some arterial rings. Carbon monoxide induced significant relaxation in precontracted human internal thoracic artery and radial artery rings. This relaxation was independent of the presence of functional endothelium in internal thoracic artery. Blocking soluble guanylate cyclase partially inhibited this relaxation, while blocking nitric oxide synthase had no effect. Carbon monoxide has a relaxing effect on human internal thoracic artery and radial artery grafts in vitro, partially via cyclic guanylate monophosphate (cGMP) pathway activation. Inducing carbon monoxide production at the cellular level in vivo in human arterial grafts might help prevent vasospasm.