Increased surface tension favors pulmonary edema formation in anesthetized dogs' lungs.

Abstract

A B S T R A C T The possibility that surface tension may affect the hydrostatic transmural pressure of pulmonary vessels and the development of pulmonary edema was studied in anesthetized, open-chested dogs.Isogravimetric pressure (the static intravascular pressure at which transmural osmotic and hydrostatic pressures are balanced such that net fluid flux is zero and lung weight is constant) was measured in nine animals under three conditions: (a) control, normal surface tension, at an alveolar pressure of 30 cm H20 with the apenic lung at room temperature; (b) after increasing surface tension by cooling and ventilating at a low functional residual capacity, at an alveolar pressure sufficient to produce the same lung volume present during control measurements; and (c) after restoring surface tension by rewarming while holding the lung at a high inflation volume, again at the control lung volume. Lung volumes were established from external dimensions and confirmed + 10% by deflation spirometry. The isogravimetric pressure (relative to alveolar pressure) was significantly less with increased surface tension than during either the initial control condition (P < 0.01), or when the surface tension has been restored (P < 0.01). Similar changes occurred in each ofthree additional studies performed with control alveolar pressures of 10 cm H20. Thus, increased surface tension favors fluid leakage presumably because it increases the microvascular transmural pressure.

Alveolar liquid pressure measured by micropuncture in isolated lungs of mature and immature fetal rabbits.

“…An increased extravascular lung water content in immature infants with surfactant deficiency (3) as well as in immature primates (4) and lambs (5) supports the experimental evidence that increased surface tension within the lungs promotes pulmonary edema (6,7). Lung fluid balance is described by the Starling equation in which penrcapillary interstitial liquid pressure is one ofthe principal forces governing fluid filtration.…”

Bronchoalveolar lavage alterations during prolonged ventilation of patients without acute lung injury

“…Surfactant abnormalities have been considered as contributing factors to ventilator-induced pulmonary oedema in animal models [22][23][24]. Besides this, it is well established that the presence of alveolar fluid, along with increased concentration of protein, especially albumin, inactivates surfactant and influences its biophysical properties [25].…”

Surfactant deficiency in rats without a decreased amount of extracellular surfactant.

“…Experimentally produced increases of alveolar surface tension have been shown to lead to pulmonary edema (25). We were therefore surprised to find less lung water in CTV-ventilated hyperthermic rats, the group that has the greatest loss of surfactant function, than in the other groups.…”