Multiple clinical and experimental studies have proved that acute renal failure (ARF) is often accompanied by injury of the remote organs including heart, lungs, liver, cerebrum, intestine. Among the extrarenal complications, the particular place belongs to the syndrome of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) associated with heavy mortality. It was also found out that the important link in ALI syndrome pathogenesis is pathology of the components of aero-hematic barrier of lungs and, in particular, type I alveolocytes. The purpose of our work was to study in dynamics the ultrastructural changes of type I alveolocytes in case of experimental acute renal failure. Material and methods. The experiments were done on 35 white male rats weighting 180-220 grams. Acute renal failure was induced by intramuscular administration of 50% glycerol water solution in dose of 10 ml per 1 kg of body mass. The sampling of lung tissue for electron microscopy study was carried out under ketamine anaesthesia in 12, 24, 72 hours after the beginning of experiment. Pieces of lung tissue were fixed in 2,5% solution of gluteraldehyde with further postfixation in 1% solution of osmium tetroxide. After dehydration, the material was poured over epon araldite. The cuts, obtained on ultramicrotome “Tesla BS-490”, were studied using electronic microscope “PEM-125K”. Results and discussion. Submicroscopically, in 12 hours after the beginning of experiment, the nuclei of most type I alveolocytes (A-I) had nucleoplasm of average electronic-optical density. The components of Golgi apparatus (GA) and granular endoplasm grid (GEG) were moderately dilated, some mitochondria were edematic. In 24 hours after the beginning of experiment, in A-I we observed the expressed phenomena of hyperhydration. Mitochondria have cleared matrix and isolated reduced cristas. Edema and disorganization of the components were observed in GA and GEG. At the same time, we observed the GEG membranes fragmentation. In 72 hours after the beginning of experiment, the phenomena of edema in A-I was maintained. Mitochondria had matrix of low electronic-optical density. GA is composed of vesicular dilated cisterns and a big quantity of vesicles. GEG components are dilated and vacuolated in some cells. Conclusions. The realized research showed that the experimental acute renal failure was accompanied by the expressed changes of submicroscopic structure of type I alveolocytes. The nature and expressiveness of the structural changes in type I alveolocytes depends on duration of endogenous factor. Perspectives for further research. Further research should be focused on correction of structural changes in type I alveolocytes in case of the experimental acute renal failure.
Keywords: lungs, type I alveolocytes, experimental acute renal failure
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