Lamellar body depletion in dogs undergoing pulmonary artery occlusion.
We have investigated the relationship between pulmonary artery occlusion (PAO) and the surfactant system of the lung by studying the ultrastructural responses of type II alveolar pneumocytes to PAO of 4-12 h duration in 16 mongrel dogs. In six of these animals, the occluded lung was allowed to reperfuse for 6 h before killing and in four animals subjected to PAO of 4 h duration, the occluded lung was ventilated with 5% CO2 balance air. PAO by itself resulted in a dramatic 80% reduction in the volumetric density of lamellar bodies (LB) in the type II cells. This resulted predominantly from a decrese in volume of the individual LB. Although reperfusion was associated with an increase in LB volume density toward normal, 6 h of reperfusion was insufficient to re-establish normal type II cellular morphology. Ventilation of the occluded lung with 5% CO2 prevented LB depletion indicating that alveolar CO2 tension may affect the release and/or synthesis of LB in type II pneumocytes.
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000473:pathology*; D002245:Carbon Dioxide; D004285:Dogs; D008170:Lung Compliance; D008854:Microscopy, Electron; D011650:Pulmonary Alveoli / Q000648:ultrastructure; D011651:Pulmonary Artery / Q000648:ultrastructure*; D011663:Pulmonary Surfactants / Q000096:biosynthesis*; D012119:Respiration
D011663:Pulmonary Surfactants; D002245:Carbon Dioxide