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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on June 30, 2004; DOI: 10.1124/jpet.104.070995

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Received for publication May 4, 2004.
Revised June 29, 2004.
Accepted for publication June 30, 2004.

Role of Prostaglandins in Mediating Differences in Human Internal Mammary and Radial Artery Relaxation Elicited by Hypoxia

Sachin A Gupte 1*, Elias A Zias 1, Mohan S Sarabu 1, Michael S Wolin 1

1 New York Medical College

* Address correspondence to: E-mail: sachin_gupte{at}nymc.edu

Abstract

The effects of hypoxia-reoxygenation on internal mammary (IMA) and radial (RA) arteries used for coronary artery bypass grafting (CABG) were examined to identify mechanisms regulating contractile function and differences that could contribute to vasospasm. Isolated endothelium-intact IMA and RA rings precontracted with KCl (30 mM) rapidly dilated to hypoxia (95% N2-5% CO2), with a greater relaxation in RA than IMA. Inhibitors of cyclooxygenase (10 µM indomethacin) and the TxA2 receptor (1 µM SQ-29548) potentiated the relaxation to hypoxia in IMA, but not RA, a response associated with increases in TxA2. Relaxation of IMA and RA to hypoxia appears to involve a calcium-reuptake mechanism inhibited by cyclopiazonic acid (0.2 mM), and it was not attenuated by a blocker of potassium channels (10 mM TEA). The recovery of force generation of IMA, but not RA, upon reoxygenation after 30 min of hypoxia was significantly reduced in the initial phase of reoxygenation by indomethacin and SQ-29548, and by endothelin receptor blocker BQ-123. Thus hypoxia relaxes IMA and RA by a postaglandin-independent mechanism potentially involving enhanced intracellular calcium-reuptake. The prostaglandin-mediated alterations of responses to hypoxia-reoxygenation seen in IMA, but not in RA, may predispose IMA to vasospasm-related complications of CABG.


Key words: Artery, Grafts, Human, Hypoxia, Prostaglandins, Surgery


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