Enhancement of Nitric Oxide Production Is Responsible for Minimal Intimal Hyperplasia of Autogenous Rabbit Arterial Grafts

Background:Vascular endothelium induces smooth muscle cell (SMC) relaxation mainly mediated by endothelium-derived nitric oxide (EDNO) and endothelium-derived hyperpolarizing factor (EDHF). It has previously been reported that functions of these endothelium factors have been greatly impaired in vein grafts. The present study was undertaken to determine whether the functions of EDNO and EDHF might be altered in artery graft.Methods and Results:In rabbits, the right carotid artery was excised and implanted in its original position as an autogenous graft (“artery graft”) and the non-operated left carotid artery served as the “control artery”. Histochemical changes, acetylcholine (ACh)-induced effects on the intracellular concentration of Ca2+([Ca2+]i) in endothelial cells, endothelium-dependent SMC hyperpolarization and relaxation, and tissue cGMP content were examined on post-operative day 28. “Artery graft” displayed a minimal amount of intimal hyperplasia. When compared with the “control artery”, it exhibited greater ACh-induced, endothelium-dependent relaxation, but the reverse was true when EDNO production was blocked. In the “artery graft” (vs. the “control artery”), basal cGMP content was greater, whereas the [Ca2+]iincrease in endothelial cells and the endothelium-dependent SMC-hyperpolarization induced by ACh were less.Conclusions:It is suggested that the [Ca2+]i-independent EDNO production covers the loss of function of endothelium-dependent SMC hyperpolarization and minimizes intimal hyperplasia caused by surgical operation in autogenous carotid artery graft.