Central role of vascular smooth muscle hyperreactivity in coronary hyperconstriction after balloon injury in miniature pigs
Autor: | Toshiaki Kadokami, Kensuke Egashira, Yuichi Ohara, Takeshi Kuga, Akira Takeshita, Hiroaki Shimokawa, Hiroshi Hata, Kouichi Kuwata |
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Rok vydání: | 1997 |
Předmět: |
Male
Serotonin medicine.medical_specialty Contraction (grammar) Vascular smooth muscle Endothelium Swine Coronary Angiography Muscle Smooth Vascular Catheterization In vivo Internal medicine medicine Animals Endothelial dysfunction business.industry General Medicine medicine.disease Coronary Vessels Disease Models Animal medicine.anatomical_structure Vasoconstriction Microscopy Electron Scanning Cardiology Swine Miniature Cardiology and Cardiovascular Medicine business Autacoid Artery |
Zdroj: | Coronary Artery Disease. 8:69-76 |
ISSN: | 0954-6928 |
DOI: | 10.1097/00019501-199702000-00001 |
Popis: | BACKGROUND Coronary constrictive responses to autacoids become augmented 1 week after balloon injury in our swine model. The present study aimed to elucidate the mechanisms of this effect. METHODS In 12 hypercholesterolaemic miniature pigs, the coronary constrictive response to serotonin was examined angiographically 1 week after injury. After the angiographic study, organ chamber experiments using excised coronary artery were performed to clarify whether functional changes in endothelial cells or in vascular smooth muscle cells contributed to the hyperconstriction. RESULTS The coronary constrictive response to serotonin in vivo was significantly greater at the previously injured site than at the non-injured site. The degree of the hyperconstriction at the previously 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 studies demonstrated that serotonin caused significantly greater contraction 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 comparable at the injured and non-injured sites. CONCLUSIONS These results suggest 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 geometric effect may be minimal. |
Databáze: | OpenAIRE |
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