Endothelium-dependent contraction and relaxation of the human and canine internal mammary artery: Studies on bypass graft vasospasm

P. J. Lin, P. J. Pearson, Hartzell V Schaff

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26 Citations (Scopus)

Abstract

The internal mammary artery (IMA) is the preferred conduit for coronary artery bypass graft because of superior late patency. However, IMA vasospasm may contribute to myocardial ischemia and early postoperative morbidity. To investigate mechanisms of vasospasm, we compared the reactivity of human and canine IMA segments in vitro to agonists known to release endothelium-derived contracting factor and endothelium-derived relaxing factor. Rings (4 mm in length) of human and canine IMA were studied in organ chambers. Human and canine vascular smooth muscle exhibited comparable contraction to norepinephrine (maximum = 7.55 ± 0.63 gm and 6.4 ± 0.90 gm, respectively) and relaxation to sodium nitroprusside. Human and canine IMAs exhibited comparable endothelium-derived relaxing factor-mediated relaxations to acetylcholine (human) and methacholine (canine). Human and canine IMA also exhibited comparable endothelium-dependent contraction to hypoxia (to 173.3% ± 8.1% and 178.9% ± 16.0% of initial prehypoxic tension; means ± SEM; n = 12). Endothelium-dependent contraction to hypoxia in human and canine IMA could be attenuated by N(G)-monomethyl-L-arginine (10-6 mol/L), a competitive inhibitor of L-arginine metabolism (n = 9 and n = 10 for human and canine; p < 0.05). These studies establish that the canine is an appropriate model for study of human IMA vascular reactivity and that hypoxia can induce the release of an L-arginine-dependent, endothelium-derived contracting factor in the human and canine IMA. In vivo, the release of endothelium-derived contracting factor in response to hypoxemia may be cause of IMA vasospasm.

Original languageEnglish (US)
Pages (from-to)127-135
Number of pages9
JournalSurgery
Volume110
Issue number2
StatePublished - 1991

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Mammary Arteries
Endothelium
Canidae
Transplants
Arginine
Endothelium-Dependent Relaxing Factors
Methacholine Chloride
Nitroprusside
Vascular Smooth Muscle
Coronary Artery Bypass
Acetylcholine
Myocardial Ischemia
Blood Vessels
Norepinephrine
Morbidity

ASJC Scopus subject areas

  • Surgery

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Endothelium-dependent contraction and relaxation of the human and canine internal mammary artery : Studies on bypass graft vasospasm. / Lin, P. J.; Pearson, P. J.; Schaff, Hartzell V.

In: Surgery, Vol. 110, No. 2, 1991, p. 127-135.

Research output: Contribution to journalArticle

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abstract = "The internal mammary artery (IMA) is the preferred conduit for coronary artery bypass graft because of superior late patency. However, IMA vasospasm may contribute to myocardial ischemia and early postoperative morbidity. To investigate mechanisms of vasospasm, we compared the reactivity of human and canine IMA segments in vitro to agonists known to release endothelium-derived contracting factor and endothelium-derived relaxing factor. Rings (4 mm in length) of human and canine IMA were studied in organ chambers. Human and canine vascular smooth muscle exhibited comparable contraction to norepinephrine (maximum = 7.55 ± 0.63 gm and 6.4 ± 0.90 gm, respectively) and relaxation to sodium nitroprusside. Human and canine IMAs exhibited comparable endothelium-derived relaxing factor-mediated relaxations to acetylcholine (human) and methacholine (canine). Human and canine IMA also exhibited comparable endothelium-dependent contraction to hypoxia (to 173.3{\%} ± 8.1{\%} and 178.9{\%} ± 16.0{\%} of initial prehypoxic tension; means ± SEM; n = 12). Endothelium-dependent contraction to hypoxia in human and canine IMA could be attenuated by N(G)-monomethyl-L-arginine (10-6 mol/L), a competitive inhibitor of L-arginine metabolism (n = 9 and n = 10 for human and canine; p < 0.05). These studies establish that the canine is an appropriate model for study of human IMA vascular reactivity and that hypoxia can induce the release of an L-arginine-dependent, endothelium-derived contracting factor in the human and canine IMA. In vivo, the release of endothelium-derived contracting factor in response to hypoxemia may be cause of IMA vasospasm.",
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