American Physiological Society

Two theories are applied to measurements of the decrease in apparent viscosity of blood in narrow tubes (Fahraeus-Lindqvist effect). First, the effect may be attributed to the presence of unsheared laminae in the fluid (sigma phenomenon), and it was found that the thickness of such laminae must vary between 3.5 µ at 10% hematocrit and 34 µ at 80%. Alternatively, the effect may be caused by a cell-free marginal zone adjacent to the tube wall, which would have to be 6 µ thick at 10% hematocrit and 1.5 µ at 80%. There is a slight suggestion in the data that the effect may be reversed as the flow rate approaches zero (i.e. the apparent viscosity rises in small tubes). Finally, a method is proposed for calculating the effective diameter of a vascular bed, and it was found to be 55 µ for a dog's hind limb.

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.

Plasma free fatty acid (FFA) turnover rates have been estimated in dogs by a technique involving measurement of FFA specific activities during constant intravenous infusion of trace amounts of C¹⁴-labeled palmitic acid. In order to determine the relationship between FFA concentration and turnover, variations in plasma FFA levels ranging from 0.081 to 3.31 µEq/ml were induced by a variety of physiological and pharmacological treatments. Calculated FFA turnover rates ranged from 2.1 to 58.8 µEq/kg/min, with a highly significant linear regression of FFA turnover on FFA level. It is concluded that under a variety of conditions changes in FFA concentration are brought about by changes in FFA production rate and that changes in FFA uptake are simple mass-action effects of changes in FFA concentration. Respiratory C¹⁴O₂ data are presented indicating that about one-fourth of the total expired CO₂ is derived from FFA in the postabsorptive state. This accounts for the immediate fate of about one-fourth of the total FFA leaving the plasma.

Male and female rats, equipped with stainless steel re-entrant tubes implanted in the brain adjacent to one preoptic area, were placed in cages with accessible activity wheels. Brain temperatures were recorded continuously for periods up to 48 hr by means of thermocouples inserted into the tubes. The activities of running, feeding, and drinking were recorded simultaneously. About 90% of feeding and drinking activity occurred irregularly during three to nine periods of running activity at night. Active periods at night were associated with brain temperatures 1.0–2.5 C higher than inactive periods during the night or day. Moderate restraint with absence of food abolished these cyclic temperature variations whereas absence of food alone did not. During the night of estrus (9 pm–3 am), marked increases in activity frequently were associated with elevated mean preoptic temperatures.

The uptake of 14C-labeled cholic, taurocholic, and chenodeoxycholic acid by the perfused rat liver was studied to characterize the mechanism responsible for hepatic uptake of bile acids. A rapid-injection multiple indicator-dilution technique and the three-compartment model of Goresky were employed. The kinetics of hepatic uptake of the three bile acids could be described by the Michaelis-Menten equation. The maximal uptake velocities (Vmax) were 24.9 +/- 2.2 (mean +/- SD), 20.8 +/- 1.2, 1.2, and 11.4 +/- 0.9 nmol/s-g liver for cholic, taurocholic, and chenodeoxycholic acid, respectively. The corresponding apparent half-saturation constants (Km) were 526 +/- 125, 258 +/- 43, and 236 +/- 48 nmol/g liver. Competitive inhibition could be demonstrated between cholate and taurocholate as well as between cholate and chenodeoxycholate. Substitution of 94% of the Na+ in the perfusion medium decreased the Vmax and the apparent Km of taurocholate uptake by 68 and 55%, respectively. These findings are consistent with the hypothesis that bile acids are taken up into the hepatocyte by Na+-dependent carrier-mediated transport.