The Application of Starling's Law of Capillary Exchange to the Lungs*

Abstract

Summary. The forces governing the movement of water across the pulmonary capillaries were studied in 39 intact, spontaneously breathing dogs. A situation favoring the net movement of water out of the pulmonary capillaries was created by means of partial pulmonary venous obstruction (left atrial balloon catheter) followed by rapid saline hemodilution. A predetermined difference between pulmonary capillary and plasma colloid osmotic pressures was maintained for periods of 1 to 2 hours. Left atrial (PLA) and plasma colloid osmotic pressures (7rp1) were measured directly. The water content of the lungs was measured serially by an indicator-dilution technique, and at autopsy by drying the lungs. The rate of accumulation of lung water was measured in four groups of animals: in three of the groups, the capillary hydrostatic and colloid osmotic pressures were varied; in the fourth group, the right lymphatic duct was obstructed in addition.The average rate of water accumulation in the lungs varied in a nonlinear way with the level of the capillary hydrostatic-plasma colloid osmotic pressure difference and was unaffected by the level of the capillary hydrostatic pressure. At low levels of PLA -7rpl, water accumulated in the lung at an average rate of 0.09 g per g dry lung per hour per mm Hg pressure difference.At higher levels of PLA -7rpl the average rate of accumulation was 0.22 g per g per hour per mm Hg AP; in most of the experiments in this group water accumulated in the lungs slowly during the first 30 minutes of the test period and more rapidly as the period was extended. Obstruction of right lymphatic duct outflow did not alter the rate of water accumulation. Based on the control data of the present experiments, the pericapillary pressure in normal lungs is estimated to be of the order of -9 mm Hg in the normal dog lung. The filtration coefficient for the pulmonary capillaries is estimated to be of the order of one-tenth to one-twentieth of that for canine muscle capillaries. The data of the present study indicate that edema formation in lung tissue cannot be defined solely in terms of intravascular forces, but may be governed to a significant degree by changes in pericapillary forces in the pulmonary interstitium.

Pulmonary Extravascular Chloride Space and Albumin Content in Adult Dogs and Puppies

“…In view of the relatively low level of pulmonary capillary hydrostatic pressure, the application of Starling's law of capillary exchange to these data indicates that interstitial hydrostatic pressure is substantially subatmospheric [12]. Although consistent with recent measurements of interstitial pressure using perforated capsules [9], this line of argument must be considered speculative because of uncertainty as to the distribution of protein in the interstitial fluid.…”

“…Two I-g portions of each lung were ground in 5 ml distilled water with a glass tissue grinder and the resulting homogenates were analyzed for I25I, 51Cr, and 36C1. T h e remainder of the lung was weighed and dried to constant weight as described previously [12] to determine total lung water.…”

Indicator dilution measurements of extravascular water in the lungs

“…Chinard has pointed out that a threshold difference between vascular pressure and plasma colloid osmotic pressure must be reached before edema formation begins around a given vessel (51); and Levine, Mellins, Senior, and Fishman have demonstrated this threshold phenomenon in the lungs (52). Our studies were carried out at levels below this threshold, at levels in which even capillary filling was incomplete, and there was no evidence for edema formation.…”

Pulmonary edema related to changes in colloid osmotic and pulmonary artery wedge pressure in patients after acute myocardial infarction.

“…Nevertheless, the reduction of colloid osmotic pressure regardless of cause would of itself facilitate transudation of fluid into the pulmonary interstitium and alveoli at relatively low left ventricular filling pressure.7 8 Since in this series measurements were performed when the patients were in pulmonary edema rather than preceding it, a cause-effect relationship between decreased colloid osmotic pressure and the development of pulmonary edema was not demonstrated. However, the data are unequivocal with respect to changes that follow treatment of pulmonary edema.…”