American Physiological Society

Effects of endotoxin on the pulmonary hemodynamics of dogs and cats have been studied in intact animals, open chest animals with and without control of cardiac output by an extracorporeal venous reservoir—pump system, and in isolated perfused continuously weighed lungs. Pulmonary artery pressure increased without a rise in left atrial pressure in all preparations following the injection of endotoxin. Pulmonary artery wedge and small pulmonary vein pressures uniformly increased. Total pulmonary vascular, pulmonary arterial and pulmonary venous resistances were calculated in five perfused lungs. The absolute increase in pulmonary venous resistance was greater than in the arterial resistance in four of the five studies and was relatively greater in every instance. There was a consistent increase in lung weight associated with these hemodynamic changes. Analysis of the determinants of lung weight changes has provided evidence to support the conclusion that the pulmonary vascular response to endotoxin administration is characterized predominantly by constriction of pulmonary venules and/or small veins.

Liver slices of ATG obese mice, of rats trained to eat their 24-hour ration in 1 hour and of rats fed a high carbohydrate diet after a 48-hour period of fasting were incubated with acetate-1-C¹⁴ and with glucose-U-C¹⁴ and the extent of incorporation of the precursor label in the fat fraction was measured. Comparatively high rates of lipogenesis were observed in all three circumstances, the highest in the ‘refed’ group. A high positive correlation was found between initial glycogen content and lipogenic performance of the slices. A high rate of glucose absorption from the g.i. tract was noted in the ‘trained’ animals. A three to fourfold increase in TPN-linked hexose monophosphate shunt dehydrogenase activity was found in preparations from the livers of ‘refed’ rats. The problem of ‘supernormal’ lipogenesis is discussed in the light of recent studies on the ‘failure’ of lipogenesis associated with diabetes and carbohydrate deprivation and the possible significance of a fluctuating supply of TPNH as a central mechanism in the adaptation and de-adaptation of the lipogenic apparatus is reemphasized.