LAMELLAR BODIES AND SURFACTANT PHOSPHOLIPIDS AFTER PULMONARY ARTERY OCCLUSION AND REPERFUSION

Abstract

22 dogs were anesthetized (sodium pentabarbital), intubated with a Carlens double lumen endotracheal tube and ventilated mechanically (Vt=15ml/kg) in the supine position. Nine animals underwent 2 to 24 hrs of balloon left pulmonary artery occlusion (LPAO), 8 had LPAO of 2 to 12 hrs followed by 6 hrs of reperfusion, and 5 served as controls. PaCO2, pH and PaO2 were maintained in the normal range. At necropsy the right and left lungs were lavaged with 0.9% NaCl and tissue was obtained for phospholipid analysis and electron microscopy (EM). Phospholipids were separated by 2 dimensional thin layer chromatography on silica gel H. Phosphatidylcholine, phosphatidyiserine, phosphatidyl inositol, phosphatidylethanolamine, phosphatidylglycerol and sphingomyelin were measured as phosphate and by densitometry.Results: 1. No animal developed atelectasis. 2. There were no qualitative differences in phospholipid composition, either between study animals and controls or between non-occluded, occluded or reperfused lungs of the same animal. 3. Depletion of lamellar bodies (LB) from type 11 pneumocytes within 2 hrs of LPAO, followed by reappearance in 12-24 hrs was demonstrated by EM. 4. Six hrs of reperfusion was associated with reappearance of LB. We conclude that LPAO produces temporary cellular depletion of LB lasting from 2 to 12 hrs and that no qualitative alterations in the phospholipid composition of tissue or alveolar wash result from LPAO.