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Endothelin-1-mediated coronary vasoconstriction deteriorates myocardial depression in hearts isolated from lipopolysaccharide–treated rats: Interaction with nitric oxide.

Authors :
Jie Tu
Qixian Shan
Hongfeng Jin
Jean-Pierre Bourreau
Qiang Xia
Source :
Clinical & Experimental Pharmacology & Physiology. Sep2004, Vol. 31 Issue 9, p571-574. 4p.
Publication Year :
2004

Abstract

1. The aim of the present study was to evaluate the contribution of disturbance of coronary perfusion to myocardial depression in hearts isolated from lipopolysaccharide (LPS)-treated rats and to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO).2. Rats were treated with LPS (10 mg/kg, i.p.) and, 4 h later, plasma ET-1 concentrations were measured by radioimmunoassay and hearts were excised for perfusion at a constant perfusion flow. The selective ETA receptor antagonist BQ-123, in the absence or presence of aminoguanidine, a specific inhibitor of inducible NO synthase, was given 15 min before LPS challenge. Coronary perfusion pressure (CPP) and measures of myocardial contractile function were recorded.3. In hearts isolated from LPS-treated rats, there was a marked increase in CPP that was abolished by pretreatment with BQ-123. In parallel, an increase in plasma ET-1 concentrations was seen in these rats. Lipopolysaccharide also induced decreases in left ventricular developed pressure (LVDP), the product of LVDP and heart rate and maximal rate of rise/fall of left ventricular pressure (+/– dP/dtmax). Single treatment with BQ-123 or aminoguanidine attenuated LPS-induced myocardial depression. However, when these two drugs were given simultaneously, myocardial depression elicited by LPS was blocked significantly.4. Endothelin-1-mediated coronary vasoconstriction, together with NO, contributes to myocardial depression in hearts isolated from LPS-treated rats. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
03051870
Volume :
31
Issue :
9
Database :
Academic Search Index
Journal :
Clinical & Experimental Pharmacology & Physiology
Publication Type :
Academic Journal
Accession number :
14689173
Full Text :
https://doi.org/10.1111/j.1440-1681.2004.04049.x