The behaviour of the granular alveocytes in chronic pulmonary congestion, pulmonary fibrosis and after extracorporeal circulation
Anyanwu, E.; Gieseking, R.; Dittrich, H.; Klinke, F.; Enders, H.J.
Der Anaesthesist 30(9): 481-488
1981
ISSN/ISBN: 0003-2417 PMID: 7283116 Document Number: 179037
The granular alveocytes, the site of the production of surfactant, undergo characteristic changes following chronic pulmonary congestion and the succeeding fibrosis, and after extracorporeal circulation. Congestion is accompanied by cell edema and the breakdown of the lamellar bodies. With fibrosis the cells are shrunken and have been, if any, lysosomes. The nuclei are pyknotic or demonstrate karyolysis. Vacuolar degeneration of the lamellar bodies and progressive degeneration of the mitochondria are observed. The extracorporeal circulation damages many granular alveocytes. The degree of damage correlates with the duration of the cardiopulmonary bypass and with the degree of the pre-pump pathological changes present in the lungs. Extracorporeal circulation induces, in intact cells, enhances surfactant production during which the different developmental stages of the lamellar body increasingly accumulate within the cell. Pulmonary congestion and fibrosis reduce the activity of the granular alveocytes. Extracorporeal circulation enhances structurally favorable conditions the granular alveocytes for the increased release of the surfactant in the immediate postoperative phase, a process which could be regarded as an autoregulatory mechanism.