Abstract

1. Liver thermogenesis was determined by measuring the oxidative metabolism of isolated perfused rat liver. 2. Metabolism of isolated liver decreases during the perfusion experiment even when perfusion conditions are maintained constant. This decrease of metabolism is caused by changed blood composition occuring in the course of its recirculation. It can be concluded that only the highest level of oxygen consumption of isolated liver measured at the beginning of the perfusion experiment or after blood exchange during the experiment corresponds to the level of resting liver metabolism in vivo. On the basis of this finding it is necessary to assume that resting liver metabolism is much higher (about 6 to 8 ml O2/g of liver/hour) than was previously thought as a result of the measurement of O2 consumption of liver slices. 3. Livers and blood of rats (Sprague-Dawley strain) acclimated to warm (30°) or cold (6° C) were used. The average resting O2 consumption of liver isolated from cold-acclimated rats (7.8 ml O2/g/hour) differs significantly from the liver O2 consumption of warm-acclimated rats (6.2 ml O2/g/hour). Therefore, liver metabolism amounts to 19.3% of the basal metabolism in warm-acclimated and to 26.5% in cold-acclimated rats. Under basal conditions livers of rats acclimated to 6° C produce about 35% more heat than livers of rats acclimated to 30° C. 4. The utilization of liver thermogenesis for thermoregulatory purposes on exposure of the organism to cold can be estimated only roughly on the basis of changes of factors affecting the liver oxidative metabolism. Oxygen consumption of isolated perfused liver depends on perfusion factors connected with supplying the liver with oxygen, the rate of liver blood flow, temperature of environment and on metabolic factors connected with the content of metabolic substrates and hormones in the perfusion medium. These factors can increase the resting oxygen consumption of the liver. 5. We assume the existence of a thermogenetic mechanism, consisting of the hormone influence on the liver metabolism via changes in substrates concentration in the blood and by blood flow changes. However, there is some evidence that the quantiative significance of this thermogenetic mechanism is restricted.

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