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PubMed1957

The effect of dinitrophenol, hypoxaemia and ischaemia on the phosphorus compounds of the dog heart.

The results reported in this paper indicate that dinitrophenol acts directly on the isolated heart, increasing its metabolic rate. It also produces heart failure associated with a low phosphocreatine content of the muscle but with no change in adenosine triphosphate, which may or may not be due to a relative hypoxia of the cardiac tissue. Experimental arterial hypoxaemia, if severe, produces a similar picture of heart failure with a decrease in phosphocreatine and no change in adenosine triphosphate. Ligation of the coronary arteries results in disappearance of the major part of the phosphocreatine within a few minutes regardless of whether or not ventricular fibrillation ensues; the adenosine triphosphate remains unchanged.

Adenosine Triphosphate↗
PubMed1957

The mechanism of dinitrophenol heart failure.

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.

Adenosine Triphosphate↗
PubMed1958

The action of nitrophenols on the metabolic rate of rats.

The effect of the mono- and di-nitrophenols and certain related compounds has been determined on the rate of oxygen consumption, the rate of carbon dioxide output and the rectal temperature of the Wistar albino rat.Of the compounds examined, only 2:4-dinitrophenol and its derivative, 3:5-dinitro-o-cresol, stimulated metabolic rate. 2-Nitrophenol and 2:3-, 2:6-, and 3:5-dinitrophenol produced no change in metabolic rate; 3-nitrophenol and 2:5-dinitrophenol had no action on carbon dioxide production although they caused a decrease in oxygen consumption. 4-Nitrophenol and 3:4-dinitrophenol increased only the rate of carbon dioxide output; 2-amino-4-nitrophenol increased the rate of carbon dioxide output and decreased the rate of oxygen consumption; 4-amino-2-nitrophenol caused depression of metabolic rate.It was confirmed that neither rectal temperature nor carbon dioxide output could replace rate of oxygen consumption as a reliable index of metabolic stimulant action. An apparatus is described which facilitates measurement of the oxygen consumption of small mammals.

Animals↗