Occurence of lipid bodies in canine type II pneumocytes during hypothermic lung ischemia

Type II pneumocytes defend the pulmonary alveolus by synthesis and secretion of surfactant and by contributing to alveolar epithelial regeneration. Lipid bodies are regarded as intracellular domains for the synthesis of eicosanoid mediators that can be induced by inflammatory stimuli. The aim of the present study was to establish whether hypothermic ischemic lung storage without further preservation measures leads to an induction of lipid body formation in canine type II pneumocytes. The lungs of 18 dogs were fixed for transmission electron microscopy (TEM) immediately after cardiac arrest (six double lungs) and after ischemic storage in Tutofusin solution at 4 degrees C for 20 min, 4 hr, 8 hr, and 12 hr (six single lungs, respectively). Type II pneumocytes were analyzed qualitatively by conventional TEM (CTEM) and quantitatively by stereology. The relative phosphorus content of surfactant containing lamellar bodies, lipid bodies, and intermediate forms was investigated by energy-filtering TEM (EFTEM). By CTEM, lipid bodies as well as forms intermediate between lipid bodies and lamellar bodies were already noted in the control group but were more pronounced in the ischemia groups. Beginning at 20 min of ischemic storage, a significant increase in the volume density of lipid bodies was noted in the ischemic groups as compared to the control group. By EFTEM, the highest intracellular phosphorus signals were recorded over lamellar bodies and lamellar areas of intermediate forms in all experimental groups, while lipid bodies and homogeneous areas of intermediate forms did not show a clear phosphorus signal. These results indicate that the formation of lipid bodies in canine type II pneumocytes is induced early during ischemic lung storage.