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Biomedical subjects

Iu A Kirillov

Publications and source records attributed to Iu A Kirillov.

13 recordsLinked to original sources
PubMed1991

[The structural changes in the lungs and the phospholipids of the pulmonary surfactant in experimental bleomycin-induced pneumosclerosis in rats].

Light microscopy was used to study rat lungs. Some morphological and biochemical characteristics after single bleomycin intratracheal administration in a dose of 10 mg/kg were studied. Some metabolic changes in the alveolar epithelium and vascular endothelium were estimated quantitatively. The peculiar picture of acute toxic alveolitis in the early stage of the injury and the features of fibrotic alveolitis by the 30-60th day were observed. The LDH and succinate dehydrogenase activities in the alveolar epithelium increased by the 3-7th day and returned to normal by the 30th day. At the same time the PL content increased 2-fold by the 30-60th day. The lysolecithin, sphingomyelin and phosphatidylserine concentration increased on the 3-7th day and returned to normal level on the 14th day. The phosphatidylglicerol content decreased significantly by the 60th day.

Animals↗
PubMed1985

[Pathomorphology of the lungs and microcirculatory bed of the lesser circulation in chronic experimental allergic alveolitis].

Granulomatous lung lesions were produced in rats by 5 intravenous or intratracheal injections of the killed BCG suspension as an antigen. On the basis of immunocomplex and cell-mediated immunopathological reactions this condition may be considered as a chronic allergic form of alveolitis. Granulomas were formed along the arteries when the antigen was administered intravenously and along the bronchi after its intratracheal administration. In both cases there were single granulomas in the alveolar septa interstitium. The microcirculatory bed was studied in semithin sections and morphometrically in thick sections after impregnation with an Indian ink and 5% gelatin. The alveolar septa capillaries in control rats were shown to form a network the parameters ow which rather correspond to the "sheet-blow" model (Fung and Sobin, 1969). In chronic allergic alveolitis, a reduction of the capillary network develops at the zone of granulomatous inflammation while in the relatively normal zone a network type of the microcirculatory bed is preformed into the main one with the formation of predominant routes of circulation that provide the blood filling of the heart cavities.

Alveolitis, Extrinsic Allergic↗
PubMed1980

[Morphogenesis of chronic pyelonephritis (electron microscopic study)].

Examinations of 51 rabbits and 86 patients with chronic pyelonephritis showed the morphogenesis of chronic pyelonephritis to be due to the effect of certain factors. One of them is the capillary-parenchymatous block resulting from the outgrowth of the connective tissue between the tubules and peritubular capillaries. Glomerular sclerosis occurs both periglomerularly (growth of the connective tissue into the capsule) and intraglomerularly (tropocollagen synthesis by mesangiaal cells). Nephrosclerosis combines diffuse sclerosis (the consequence of increasing hypoxia) and focal sclerosis (the consequence of renal tissue destruction during pyelonephritis attacks) which determine the features of regenerative hypertrophy of nephrons and the pattern of pyelonephritic shrinking of the kidney.

Adult↗
PubMed1979

[Morphogenesis of acute pyelonephritis (electron microscopic study)].

Investigations of fine changes of nephron elements in acute pyelonephritis against the background of urolithiasis in 19 patients and 43 rabbits showed the developing morphological lesions in the kidneys to be due to combined effect of the inflammatory and ischemic factors. The inflammation began with the development of serous oedema leading to destruction of tubular epithelium and impairment of urine passage. These lesions contributed to transformation of the serous inflammation into purulent one with formation of histolysis foci. The ischemic factor progressed with the advance of the inflammatory process and was aggravated by the development of foci of histolysis and hephrohydrosis and subsequently of vascular-parenchymatous block at the tubular level.

Acute Disease↗