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British Journal of Pharmacology and Chemotherapy logoLink to British Journal of Pharmacology and Chemotherapy
. 1957 Sep;12(3):273–278. doi: 10.1111/j.1476-5381.1957.tb00134.x

The mechanism of dinitrophenol heart failure

G Fawaz, B Tutunji
PMCID: PMC1509687  PMID: 13460230

Abstract

Hypoxaemia, resulting from increased tissue metabolism, is an important factor in dinitrophenol failure in the conventional heart-lung preparation. Improved oxygenation of the blood by a technique described in this paper prolongs the life of dinitrophenol-treated hearts. Dinitrophenol acts very rapidly; oxygen consumption and coronary flow increase in a few minutes and the increase is proportional to the dose. The increase in oxygen consumption diminishes with time. Dinitrophenol decreases the phosphocreatine content of the heart, even when there is no failure or hypoxia. There is no evidence that dinitrophenol failure can be due to a decrease of phosphocreatine or adenosine triphosphate content of the heart, although this is to be expected in view of the observed “uncoupling” action of dinitrophenol.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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