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The Journal of Thoracic and Cardiovascular Surgery, Vol 97, 259-266, Copyright © 1989 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
GW He, B Buxton, FL Rosenfeldt, AC Wilson and JA Angus
The function of beta-adrenoceptors in the human internal mammary artery was
studied in vitro to predict the way in which the internal mammary artery
graft would respond to beta-adrenergic agonists and antagonists given in
the perioperative period. Ring segments of the distal internal mammary
artery obtained from patients not receiving beta-blocker therapy were
mounted in organ baths and isometric wall force was measured. For
comparison, similar experiments were conducted on segments of canine
coronary artery, a vessel known to have powerful beta-adrenoceptor
function. All arteries were precontracted with potassium or the thromboxane
mimetic agent, U46619, before isoproterenol cumulative
concentration-relaxation curves were constructed. In the human internal
mammary artery, the maximum relaxation induced by isoproterenol was only
14% of the potassium- induced contraction and 24% of the U46619-induced
contraction. These responses were weak compared with 54% and 86% for
beta-adrenoceptor relaxation measured in corresponding experiments in the
canine coronary artery. In all experiments, propranolol antagonized the
relaxation induced by isoproterenol. These studies suggested that the human
internal mammary artery has only a small number of beta-adrenoceptors. We
conclude that beta-adrenoceptors would contribute little to the reactivity
of the human internal mammary artery graft to sympathomimetic drugs.
ARTICLES
Weak beta-adrenoceptor-mediated relaxation in the human internal mammary artery
Baker Medical Research Institute, Melbourne, Australia.
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