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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Effect of the effluent released from the canine internal mammary artery after intraluminal and extraluminal perfusion of acetylcholine and adenosine diphosphate

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Author(s):
Matsuda, Nilce Mitiko [1] ; Pearson, Paul J. [2] ; Schaff, Hartzell V. [2] ; Piccinato, Carlos E. [1] ; Rodrigues, Alfredo J. [1] ; Barbosa Evora, Paulo Roberto [1]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Surg & Anat, Sao Paulo - Brazil
[2] Mayo Clin Fdn, Div Cardiovasc Surg, Rochester, MN - USA
Total Affiliations: 2
Document type: Journal article
Source: JOURNAL OF BIOMEDICAL SCIENCE; v. 16, MAY 5 2009.
Web of Science Citations: 1
Abstract

Segments of the canine internal mammary artery (35 mm in length) were suspended in vitro in an organ chamber containing physiological salt solution (95% O(2)/5% CO(2), pH = 7.4, 37 degrees C). Segments were individually cannulated and perfused at 5 ml/minute using a roller pump. Vasorelaxant activity of the effluent from the perfused internal mammary arteries was bioassayed by measuring the decrease in tension induced by the effluent of the coronary artery endothelium-free ring which had been contracted with prostaglandin F(2 alpha) (2 x 10(-6) M). Intraluminal perfusion of adenosine diphosphate (10(-5) M) induced significant increase in relaxant activity in the effluent from the perfused blood vessel. However, when adenosine diphosphate (10(-5) M) was added extraluminally to the internal mammary artery, no change in relaxant activity in the effluent was noted. In contrast, acetylcholine produced significant increase in the relaxant activity on the effluent of the perfused internal mammary artery with both intraluminal and extraluminal perfusion. The intraluminal and extraluminal release of endothelium-derived relaxing factor (EDRF) by acetylcholine (10(-5) M) can be inhibited by site-specific administration of atropine (10(-5) M). These experiments indicate that certain agonists can induce the release of EDRF only by binding to intravascular receptors while other agonists can induce endothelium-dependent vasodilatation by acting on neural side receptors. (AU)