Endothelial vasodilator function is preserved at the spastic/inflammatory coronary lesions in pigs

Kenji Miyata, Hiroaki Shimokawa, Tohru Yamawaki, Ikuko Kunihiro, Xuchen Zhou, Taiki Higo, Eriko Tanaka, Naoki Katsumata, Kensuke Egashira, Akira Takeshita

研究成果: Contribution to journalArticle査読

28 被引用数 (Scopus)

抄録

Background - The question of whether or not endothelial vasodilator function in the spastic coronary artery is preserved is still controversial. We recently developed a porcine model in which long-term and local treatment with interleukin-1β (IL-1β) from the adventitial site causes coronary arteriosclerotic changes and vasospastic responses to autacoids. The aim of this study was to examine the endothelial vasodilator function in our new porcine model of the spasm both in vivo and in vitro. Methods and Results - A segment of the porcine coronary artery was aseptically wrapped with cotton mesh that held absorbed IL-1β-bound microbeads. Two weeks after the procedure, intracoronary administration of serotonin caused coronary vasospasm at the IL-1β-treated site (n = 10). Coronary vasodilatation to bradykinin, substance P, or an increase in coronary blood flow was preserved at the spastic site. Vasodilator responses to 3-morpholinosydnonimine (an NO donor) and nitroglycerin also were comparable between the 2 sites. The vasoconstricting response to N(G)-monomethyl-L-arginine and the extent of the augmentation of the serotonin-induced vasoconstriction were comparable between the 2 sites. Organ chamber experiments showed that endothelium- dependent relaxations to bradykinin, the calcium ionophore A23187, and even the vasospastic agonist serotonin were preserved at the spastic site, whereas contractions to serotonin were augmented at the spastic site regardless of the presence or absence of the endothelium (n=6). Endothelium-independent relaxations to sodium nitroprusside were also preserved at the spastic site. Conclusions - These results indicate that endothelial vasodilator function is preserved at the spastic site and that the spasm is caused primarily by smooth muscle hypercontraction in our porcine model.

本文言語英語
ページ(範囲)1432-1437
ページ数6
ジャーナルCirculation
100
13
DOI
出版ステータス出版済み - 9 28 1999

All Science Journal Classification (ASJC) codes

  • 循環器および心血管医学
  • 生理学(医学)

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