The University of Southampton
University of Southampton Institutional Repository

Opposite effects of nitric oxide and nitroxyl on postischemic myocardial injury

Ma, Xin L., Gao, Feng, Liu, Gao-Lin, Lopez, Bernard L., Christopher, Theodore A., Fukuto, Jon M., Wink, David A. and Feelisch, Martin (1999) Opposite effects of nitric oxide and nitroxyl on postischemic myocardial injury Proceedings of the National Academy of Sciences, 96, (25), pp. 14617-14622. (doi:10.1073/pnas.96.25.14617). (PMID:10588754).

Record type: Article


Recent experimental evidence suggests that reactive nitrogen oxide species can contribute significantly to postischemic myocardial injury. The aim of the present study was to evaluate the role of two reactive nitrogen oxide species, nitroxyl (NO(-)) and nitric oxide (NO(.)), in myocardial ischemia and reperfusion injury. Rabbits were subjected to 45 min of regional myocardial ischemia followed by 180 min of reperfusion. Vehicle (0.9% NaCl), 1 micromol/kg S-nitrosoglutathione (GSNO) (an NO(.) donor), or 3 micromol/kg Angeli's salt (AS) (a source of NO(-)) were given i.v. 5 min before reperfusion. Treatment with GSNO markedly attenuated reperfusion injury, as evidenced by improved cardiac function, decreased plasma creatine kinase activity, reduced necrotic size, and decreased myocardial myeloperoxidase activity. In contrast, the administration of AS at a hemodynamically equieffective dose not only failed to attenuate but, rather, aggravated reperfusion injury, indicated by an increased left ventricular end diastolic pressure, myocardial creatine kinase release and necrotic size. Decomposed AS was without effect. Co-administration of AS with ferricyanide, a one-electron oxidant that converts NO(-) to NO(.), completely blocked the injurious effects of AS and exerted significant cardioprotective effects similar to those of GSNO. These results demonstrate that, although NO(.) is protective, NO(-) increases the tissue damage that occurs during ischemia/reperfusion and suggest that formation of nitroxyl may contribute to postischemic myocardial injury.

Full text not available from this repository.

More information

Published date: 7 December 1999
Organisations: Clinical & Experimental Sciences


Local EPrints ID: 337879
ISSN: 0027-8424
PURE UUID: 0621e290-a96c-46aa-a695-824af0a79956
ORCID for Martin Feelisch: ORCID iD

Catalogue record

Date deposited: 29 Jun 2012 11:01
Last modified: 18 Jul 2017 06:00

Export record



Author: Xin L. Ma
Author: Feng Gao
Author: Gao-Lin Liu
Author: Bernard L. Lopez
Author: Theodore A. Christopher
Author: Jon M. Fukuto
Author: David A. Wink
Author: Martin Feelisch ORCID iD

University divisions

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton:

ePrints Soton supports OAI 2.0 with a base URL of

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.