Cable D G, Caccitolo J A, Pfeifer E A, Daly R C, Dearani J A, Mullany C J, O'Brien T, Orszulak T A, Schaff H V
Department of Laboratory Medicine and Pathology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
Ann Thorac Surg. 1999 Apr;67(4):1083-90. doi: 10.1016/s0003-4975(99)00130-7.
The extent to which the endothelium regulates radial artery (RA) contractions is unknown. The goals of this study were to characterize endothelium-dependent relaxations in the RA, compare these responses with those in the internal mammary artery (IMA), and, subsequently, manipulate nitric oxide production in the RA with adenovirus-mediated gene transfer.
Segments of RA and IMA from 43 patients were studied initially in organ chambers. Endothelial function was evaluated and gene transfer, was examined.
After precontraction to 80% maximum tension with prostaglandin F2alpha, acetylcholine produced lesser relaxations in the RA (21.5%+/-5.8%) than in the IMA (66.7%+/-10.6%); human thrombin and adenosine 5'-diphosphate yielded similar results. Reduced relaxations in the RA (16.8%+/-4.2%) compared with those in the IMA (71.6%+/-11.9%) were noted with calcium ionophore. Superfusion bioassay demonstrated a similar baseline release in both arteries but a reduced stimulated production of vasoactive substances in the RA, results confirmed by cyclic guanosine monophosphate level determination. The RA produced less 6-keto-prostaglandin F1alpha than the IMA. Light microscopy demonstrated an intact endothelium in both arteries. Adenovirus-mediated gene transfer of nitric oxide synthase augmented relaxations of the RA to acetylcholine.
Reduced production of endothelium-derived relaxing factors suggests diminished endothelial regulation of vascular smooth muscle in the RA compared with the IMA. This finding may explain, in part, the predisposition to vasoconstriction in RA grafts.
