CENTRAL ROLE OF VASCULAR SMOOTH-MUSCLE HYPERREACTIVITY IN CORONARY HYPERCONSTRICTION AFTER BALLOON INJURY IN MINIATURE PIGS

Background Coronary constrictive responses to autacoids become augment ed 1 week after balloon injury in our swine model. The present study a imed to elucidate the mechanisms of this effect. Methods In 12 hyperch olesterolaemic miniature pigs, the coronary constrictive response to s erotonin was examined angiographically 1 week after injury, After the angiographic study, organ chamber experiments using excised coronary a rtery were performed to clarify whether functional changes in endothel ial cells or in Vascular smooth muscle cells contributed to the hyperc onstriction. Results The coronary constrictive response to serotonin i n vivo was significantly greater at the previously injured site than a t the non-injured site. The degree of the hyperconstriction at the pre viously injured site exceeded that predicted from a geometric theory, Histological examination demonstrated that the previously injured site was almost covered with regenerated endothelial cells. In vitro studi es demonstrated that serotonin caused significantly greater contractio n in coronary artery strips, whether with or without endothelium, from the previously injured site than in those from the non-injured site. Endothelium-dependent relaxation in response to serotonin was comparab le at the injured and non-injured sites. Conclusions These results sug gest that the coronary hyperconstriction response to serotonin 1 week after injury results primarily from hyperreactivity of vascular smooth muscle, Whereas any contribution of endothelial dysfunction or the ge ometric effect may be minimal.