PMID: 7541961Jun 1, 1995Paper

Endotoxin-induced contractile dysfunction in guinea pig hearts is not mediated by nitric oxide

The American Journal of Physiology
U K DeckingJ Schrader

Abstract

The decreased contraction amplitude of isolated cardiac myocytes from guinea pigs exposed to lipopolysaccharide (LPS) was reported to be partially reversed by nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS) [Brady, et al., Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1963-H1966, 1992]. We have tested the potential involvement of NO formation in LPS-induced cardiac depression in the intact heart. Isolated perfused hearts of LPS-treated guinea pigs (4 mg/kg 4 h before organ removal) displayed a greatly decreased left ventricular pressure (LVP) when compared with untreated controls (48 +/- 11 vs. 93 +/- 18 mmHg, n = 6 hearts each), whereas heart rate and coronary flow were similar. Perfusion of LPS-treated hearts with L-NMMA or L-NAME (100 microM each) at constant flow did not increase LVP (50 +/- 14 and 44 +/- 11, respectively, vs. 52 +/- 14 mmHg). However, coronary resistance increased significantly. There was no difference between LPS-treated and control hearts in venous adenosine release (104 +/- 58 vs. 133 +/- 86 pmol.min-1.g-1). Measurement of the activities of the induced (iNOS) and constitutive forms of NOS revealed that there was no difference in total NOS activity (237 +/- 82 vs. 18...Continue Reading

Citations

Feb 12, 1998·British Journal of Pharmacology·G KojdaE Noack
Apr 26, 2000·American Journal of Physiology. Endocrinology and Metabolism·M J BennettR D Evans
Mar 1, 2003·American Journal of Physiology. Heart and Circulatory Physiology·Zvezdana Z KojicUlrich K M Decking
Aug 3, 2000·American Journal of Physiology. Heart and Circulatory Physiology·D B CowanF X McGowan
Oct 14, 2003·Journal of Applied Physiology·Tetsuya TatsumiMasao Nakagawa

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