Relationship of pleural effusions to increased permeability pulmonary edema in anesthetized sheep.

Abstract

We studied anesthetized sheep to determine the relationship between increased permeability pulmonary edema and the development and mechanism of pleural effusion formation. In 12 sheep with intact, closed thoraces, we studied the time course of pleural liquid formation after 0.12 ml/kg i.v. oleic acid. After 1 h, there were no pleural effusions, even though extravascular lung water increased 50% to 6.0±0.7 g/g dry lung. By 3 h pleural effusions had formed, they reached a maximum at 5 h (48.5±16.9 ml/thorax), and at 8 h there was no additional accumulation of pleural liquid (45.5±16.9 ml). Morphologic studies by light and electron microscopy demonstrated subpleural edema but no detectable injury to the visceral pleura, suggesting that the pleural liquid originated from the lung and not the pleura. In nine sheep, we quantified the rate of formation of pleural liquid by enclosing one lung in a plastic bag. By comparing in the same sheep the volume of pleural liquid collected from the enclosed lung to the volume found in the opposite intact chest, we estimated the rate of liquid absorption from the intact chest to be 0.32 ml/(kg. h); we had previously reported a liquid absorption rate of 0.28 ml/(kg. h) in normal sheep. These studies also supported the conclusion that the majority of the pleural liquid originated from the lung because we could account for all of the pleural liquid that was formed and cleared. The volume of pleural liquid collected from the enclosed lungs was equal to 21% of the excess lung liquid that formed after oleic acid-induced lung injury. Thus, the pleural space and parietal pleural lymphatic pathways are important pathways for the clearance of pulmonary edema liquid after experimentally induced increased permeability pulmonary edema.

Resolution of Pulmonary Edema. Thirty Years of Progress

“…However, in the 1980s, a combination of in vivo and in vitro studies demonstrated that the primary mechanism driving the resolution of alveolar edema was vectorial transport of sodium into the interstitial space, thereby creating an osmotic gradient for absorption of water from the distal airspaces of the lung (7). Several investigators demonstrated that the excess interstitial fluid was cleared by lung lymphatics, and by bulk flow across the low-resistance visceral pleura into the pleural space (1,8). A negative interstitial pressure gradient, even under conditions of edema, was shown to be the major force for the removal of interstitial edema fluid into lung lymphatics and the mediastinum (9).…”

Advances in Understanding of the Pathogenesis of Acute Respiratory Distress Syndrome

“…These have not been supported by data. Our understanding progressed when several investigators, working both in vivo and in vitro, demonstrated that excess interstitial fluid was cleared by a combination of lung lymphatics and bulk flow across the visceral pleura to the pleural space [113], driven by active transport of sodium into the interstitial space [114]. This is driven by Na/K-ATPase situated at the basolateral surface of the epithelial cell, generating a gradient to facilitate sodium entry at apical cell surface sodium channels.…”

Zymosan priming protects rats against pulmonary oxygen toxicity

“…They originate as a proteinaceous plasma exudate that accumulates in the lung interstitium and traverses the visceral pleura to enter the pleural space [22,23]. This study found that zymosan priming prevented the development of pleural effusions in hyperoxic rats (Table 1, ZP group).…”