Effects of Pulmonary Artery Ligation on Pulmonary Surfactant and Pressure-Volume Characteristics of Dog Lung

Abstract

The surface tension of extracts from normal lungs is extremely low owing to the presence of a specific surfactant. 1 Experiments of Finley et al. 2 showing an abnormally high surface tension of lung extracts obtained 12 to 16 hours after ligation of the pulmonary artery (PA) were confirmed by Long and associates. 3 These studies suggested that the surfactant is decreased or absent after PA ligation.The present studies were designed to correlate the pressure-volume characteristics of the lung with changes in the surface tension of lung extracts and to investigate the long term effects of PA ligation. Surface tension measurements of the lung extracts, pressurevolume curves and histological studies of lungs were made in one group of dogs four hours after the pulmonary artery was ligated and in another group of dogs two weeks after the pulmonary artery was ligated. A comparative study was also made of the results obtained by two different methods of surfactant extraction and by two different methods of surface tension measurements. MethodsThe right PA was ligated in each of 12 healthy mongrel dogs weighing 14 to 17 kg. Surgery and experimental measurements were done under thiopental (Pentothal) anesthesia. Respiration was controlled with a positive pressure respirator, administering 100% oxygen through an endotracheal tube until the PA ligation was completed (20 to 30 minutes). The dog was ventilated with room air for the remainder of each experiment. A right lateral thoracotomy was performed through the fourth intercostal space and the thoracic cavity widely exposed. Four hours after ligation of the right pulmonary artery, separate pressure-volume measurements of each lung were performed in the following manner: The indwelling endotracheal tube was connected to a three-way Luer lock stopcock with one arm leading to a calibrated 100 ml syringe and the other to a water manometer. A noncrushing clamp was applied to one main stem bronchus and the lung to be tested was inflated with air until all the lung units appeared grossly distended. The lung was then allowed to deflate passivelv. This was repeated two or three times and further volume-Dressure studies were made using the retained lung volume at zero transpulmonarv pressure (atmospheric pressure) as the base line for the volume measurements.The lung was inflated with 100 ml increments of air and the pressure changes were recorded after stabilization of the transpulmonary pressure (15 to 20 seconds). Inflation was continued seriatim until all the lung units appeared distended. The right lung which had the PA ligated, was studied first and the maximum pressure was recorded when the right lung was distended and the pressure produced in the intact lungs was kept in a comparable range. Most lungs were completely inflated when transpulmonary pressure reached approximately 40 cm H 2 O. Inflation was more irregular and more undistended units were observed during inflation in lungs two weeks after PA ligation than in the intact lungs. Deflation was performed by stepwise remo...

Lamellar body depletion in dogs undergoing pulmonary artery occlusion.

“…2) (8). Although this observation was confirmed by other investigators (9,10,30), it subsequently has been shown that blood or plasma also impairs the surface tension lowering capabilities of normal lung extracts (11,12). Subsequently, deflation pressure volume curves, alveolar bubble stability, and phospholipid contents were shown to be normal in morphologically normal regions of dog lungs with PAO (13,14).…”

“…As the duration of occlusion increases, the addition of CO2 to the inspired gas is no longer capable of reversing the decrease in compliance and ventilation to the occluded lung (8). This irreversibility coincides with the development of atelectasis, hemorrhage, and edema in the occluded lung, which in turn has been attributed to loss ofthe alveolar surface lining material, surfactant (8)(9)(10). Although the ability of pulmonary surfactant to reduce surface tension is decreased after pulmonary artery occlusion, it remains unclear whether this alteration in function contributes to the development or results as a consequence of the alveolar edema and hemorrhage that occur (8,(11)(12)(13).…”

Respiratory mechanics and gas exchange in postobstructive pulmonary vasculopathy

“…The length of time that hypocapnic bronchoconstriction persists after ligation is unknown, but it probably depends on the speed and extent of neovascularization of the lung by bronchial collaterals [3]. Of greater importance, within 2 days of ligation areas of the affected lung become atelectatic and its total lung volume is reduced by 40-50% [11,19,20]. The proportion of total ventilation directed to that lung is probably reduced below 30%, but no data are available in the literature for this postligation time period.…”

Surface tension, metabolic activity, and lipid composition of alveolar cells in washings from normal dog lungs and after pulmonary artery ligation

“…This procedure has been a useful experimental model for the study of altered pulmonary surface activity (6)(7)(8). Our aims were to: (1) localize the distribution of surface activity in the supernatant and sedimentary fractions of the wash fluid from lungs; (2) correlate the lipid composition of these fractions with their relative surface activity; (3) assess the possible role of the alveolar cells in synthesizing or storing sur-…”