Ultrastructural glomerular alterations in experimentally induced neurotoxin shock in rats.
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Biomedical subjects
Publications and source records attributed to W Drommer.
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Homogenized lung tissue was used to experimentally reproduce lethal viral pneumonia in guinea pigs. The resultant lesions corresponded with those of the spontaneous disease. Pneumonia with necrotic bronchiolar epithelium accompanied by basophilic intranuclear inclusion bodies was the primary finding. With transmission electron microscopy, numerous viral particles were found--mainly within the nucleus of pulmonary epithelial cells but also within the cytoplasm and in extracellular space. The appearance of viral particles, in particular their paracrystalline and crystalline deposition within the nucleus, indicates that our experimentally induced pneumonia was caused by an adenovirus.
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The renal corpuscles of 28 specific-pathogen-free Wistar rats fixed by perfusion were examined light microscopically and morphometrically following experimental protracted neurotoxin shock. The mean diameter of the center sections of 420 renal corpuscles was 113.0 micrometers. The mesangial portion occupied 9.5% of the total area of the renal corpuscle in control rats and increased to a maximum of 17.25% in experimental rats. The number of mesangial nuclei per renal corpuscle in rats with protracted shock showed that expansion of the mesangium with compression of capillary loops was not caused solely by an increase in the number of cells. Furthermore, there was an enlargement of the mesangial cytoplasm and matrix. Activation and proliferation of connective tissue in rats with protracted shock could be observed in the interstitium of various organs as well as in the mesangium of the glomerulus.
Severe polyarthritis was induced in 42 SPF piglets by subcutaneous and intraarticular infection in one joint of the bacterium Erysipelothrix rhusiopathiae (Serotype B, strain T 28), which in its chronic stage morphologically resembles human c.P. The light and electron microscopic examination of the articular cartilage and synovial membrane reveals a parallel evolution of hyaline cartilage degeneration, and activation and proliferation of synovial lining cells. The initial cartilage alteration with demasking of collagen fibrils and focal degeneration of chondrocytes in the erysipelas model is caused by direct action of the microbial agent, fibrin and few granulocytes Erysipelothrix bacteria and neutrophilic granulocytes are able to invade the superficial and intermediate cartilage layers. This model is not considered a suppurative infectious arthritis. In chronic villous erysipelas polyarthritis, which develops without the presence of neutrophils in the cartilage, the invasively growing synovial pannus dominates, which deeply destroys the pre-damaged cartilage, resulting in macroscopic focal or wide-spread cartilage erosion. We consider the poorly vascularized cartilage and the particular fibrosis suitable sites for the extremely long (up to three years) persistence of this microbial agent. The persistence of the agent is considered necessary for the persisting immunological reactions and the perpetuation of erysipelas polyarthritis. With longer duration (1-3 years) of experimental erysipelas polyarthritis the number of bacteriologically positive arthritic joint decreases. Microscopically, the causative bacteria may only sporadically identified.
Glomeruli of control and shock-treated, 6-8-week-old pigs (n = 16 specific pathogen-free) were analyzed by light microscopy, transmission electron microscopy and morphometry. In eight of the animals the shock was induced using a neurotoxin of the E. coli serotype O 139: k82 (B). The animals were killed 47 to 264 hours post injection. In semithin sections a significant mesangial widening and increase of the mesangial nuclei count was demonstrated. The volume of the mesangium was 11.1% in the control animals and increased to 19.6% after protracted shock. By electron microscopy we ascertained a distinct activation of the mesangial cells concomitant with an increase of ribosomes, rough endoplasmatic reticulum, lysosomes and a fusion of the epithelial pedicles. The surrounding mesangial matrix was enlarged. In this paper the significance of this mesenchymal reaction in relation to shock situations is discussed.
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Göttingen miniature pigs were used to test a combination of the active principles coumarin and troxerutin (Venalot) for teratogenic and embryotoxiic side-effects. The experimental group consisted of 17 mother pigs with 95 fetuses, the control group of 6 untreated sows with 45 fetuses. The combination of coumarin and troxerutin was administered orally at a level of the 100-fold therapeutic dose (i.e. 25 mg coumarin + 150 mg troxertutin/kg/day) from day 6 to day 30 of gestation. The pathological and histological examinations of the uteri and fetuses revealed no indications of any embryotoxic or teratogenic damage caused by the tested combinations. Morphological and clinico-chemical investigations did also not result in any findings definitely attributable to the medication.
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