Experimentelle Pathologie最新文献

Rats pregnant for 16 or 19 days (ED 16 or 19) were irradiated with 100 r and killed after 24 hrs or at age 24 or 180 days. The primary influence of X-rays consists in a lethal lesion of cells located in the periventricular zone as well as some of the more differentiated cells in the brain parenchyma. After irradiation on ED 16, the acute damage was greater in the cerebral cortex and the superior colliculus (SC) than in the lateral geniculate nucleus (LGN). Irradiation on ED 19 damaged mainly the cortical part of the visual system. The degree of acute damage is therefore inversely proportional to the degree of histo- and cytodifferentiation of the visual centres (Brückner et ai. 1976).

In adult animals the acute radiation damage results in a deficit in packing density and the total number of neurons. Animals irradiated on ED 16 revealed more pronounced changes in deep layers of the cortex (L VI) than in the superficial layers. The deficit was smaller in the SC, and in the LGN an increase in the packing density of nerve cells was found. In animals irradiated on ED 19, the deficit in neurons density occurred mainly in more superficial layers of the cortex, with a maximum deficit in layer IV.

From comparison of acute and final changes it may be concluded that the damage of preneuroblastic cell populations is compensated during later embryonic development, while the damage induced in populations already at early neuroblast stage is irreversible and leads to a permanent deficit.

Glia cell population is altered in a similar way as the number of neurons in regions poor in myelin, while in regions rich in myelin the number of glia cells seems to depend on changes in the number of efferent and afferent nerve fibres.

Proliferation of ducts was described in late stages of experimental pancreatitis induced by sodium taurochlorate solution in the guinea pig. Some of the proliferating ducts were seen in close proximity of the remaining acini. The observation suggests that acinar cells might be precursors of ductal cells through metaplasia.

The effect of chronic ethanol intoxication on oxidative phosphorylation in the rat brain mitochondrial fraction was examined. Moreover, electron microscopy was used to verify the quantitative composition of the fraction and for examination of ultrastructural changes in the mitochondria.

The experiments were carried out with 60 rats receiving, beside the normal diet, ethyl alcohol according to a modified Ratcliffe model.

In isolated rat brain mitochondria the NAD-dependent oxidation of substrates (glutamate + malate) was decreased. The phosphorylation index ADP/0 and the respiratory control ratio (RCR) in rat brain mitochondria from ethanol-treated rats were unchanged in the presence of both succinate and glutamate + malate. Chronic ethanol feeding did not induce any changes of succinate dehydrogenase and cytochrome oxidase activities in solubilised mitochondrial fractions of rat brain.

Electron microscopy studies revealed that mitochondria from control animals retained their outer and inner membranes, whereas those from rats given ethanol were almost always swollen and some were disrupted. In mitochondrial fractions isolated from ethanol-intoxicated rats an increase was observed of contaminating elements i.e. axons and synaptosomes of various sizes. It should be stressed that the mitochondria located inside synaptosomes and axons were unchanged.

The composition of the fractions was quantitively evaluated and confirmed the diminution of “free” mitochondria in the experimental fractions in favour of “bound” mitochondria which mainly occurred in the synaptosomes with preserved metabolic activity.

On the basis of electron microscopy studies it could be suggested that ethanol intoxication causes the damage of some mitochondria, which become more sensitive to mechanical destruction during isolation procedure, and they do not sediment together with the fraction of normal ones.

The absence of “free” mitochondria in pellets explains the spurious lack of disturbances in the energy metabolism of brain mitochondria after chronic ethanol intoxication.

The morphology of the spleen white pulp in DBA/2 mice bearing the chemically induced mastocytoma, P-815-X2, was evaluated by using the standardized reporting system previously introduced to describe the spleen morphology in relation to immunological functions. Special emphasis was placed on the assessment of the T- and B-lymphocytes, the appropriate functions of which have previously been proposed to be affected by the tumor concerned.

When compared with the control mice, both the central perarterial lymphoid sheaths (C-PALS) and peripheral periarterial lymphoid sheaths (P-PALS) T- and B-cell areas, respectively, were seem to be altered in a way suggesting derangement in the function of both these lymphocyte populations, almost exclusively in mastocytoma-bearing mice. The present results, thus, confirm the observations made earlier on the immunosuppressive potentialities of mastocytoma in DBA/2 mice, and the recording system used seems to be a suitable one to be applied in the evaluation of the morphologic manifestations of these immunological functions.

Cell proliferation in adenocarcinomas induced in the rat's colon by parenteral injection of 1,2-dimethylhydrazine was compared with that in normal colonic epithelium by means of autoradiographs. The distinct zone of proliferation, typical of the intestines, was not observed in the tumours, and cells replicated nearly in all segments of neoplasms. Tumour enterocytes were found to have a longer short mitotic cycle (16 instead of 11 hrs), due, chiefly, to an extension of G₁-period duration. They were also characterized by a more pronounced heterogeneity as far as the values of t_s and t_G2 are concerned, and, probably, by the formation of an R₂-population. Both the index of S-phase (29 %) and labelled cell fraction (87 %) after 6 injections of ³H-thymidine spaced at six-hour intervals, were lower in adenocarcinomas than in the zone of maximum proliferation in the descending colon (45 and 100 %, respectively) and yet higher than the same parameters calculated for the whole population of the intestinal epithelium (17 and 60%, respectively). As far as proliferation parameters go, adenocarcinoma cells highly resemble those of the crypt bottom population in control animals, which was found to consist of several subpopulations with a varying mean duration of the mitotic cycle, and where stem enterocytes are likely to occur. When enterocytes become malignant, disturbances in their differentiation decrease cell shedding into the intestinal lumen and, thus, cause tumours to arise and develop.

Fluorescent histochemical investigations were carried out on the adrenergic terminal plexus in the salivary gland of the rat 24 hours, 72 hours, and 14 days after ligation of the main excretory duct and the concomitant administration of isoproterenol (IPR, 60 mg/kg body weight subcutaneously). The atrophy of the salivary gland occurring after ligation was also present after the concomitant administration of IPR which induces amylase secretion and DNA synthesis in intact salivary glands. The adrenergic fibres in the atrophic gland exhibited an intensive fluorescence of the adrenergic terminal plexus after IPR treatment. Thus the presynaptic elements remain intact, although the acini are atrophic, and the reason for the absence of the stimulus response probably lies in the effector cells.

Previous studies have identified the bronchial Clara cell as the progenitor of the lung tumors induced in European hamsters by nitrosoheptamethyleneimine (NHMI). Using stereological methods, we compared the ultrastructure of Clara cells from untreated animals and lung tumor cells, induced by NHMI, in the European hamster. The composition and volume of the cytoplasm was significantly altered in the tumor cells whereas their nuclei did not show any measurable changes in size or structure when compared with the controls.

The aim in view was to establish whether chronic administration of ethanol causes ultrastructura changes in the brain of rats, particularly in the structures through which alcohol penetrates to the brain, that is the cerebral cortex capillaries. The experiments were performed with 5 Wistar rats, three of which received ethanol according to Ratcliffe's model for 8 weeks in increasing concentrations from 2.5 to 25 per cent. Two rats served as control. In the endothelium of some capillaries of the brain cortex in the rats ingesting ethanol an enlargement of the cell nuclei was observed.

The number of mitochondria in the cytoplasm and of micropinocytic vesicles was found to increase, and proliferation of the smooth endoplasmic reticulum and Golgi system were noted. Considerable oedema was observed in the astrocytic processes surrounding the vessels, with the presence of numerous mitochondria of abnormal shape and huge size. Oedema of perivascular astrocytic processes and enhanced pinocytosis seem to indicate an increased permeability of the blood-brain barrier as the result of the toxic effect of ethanol.

The peculiarities of enterocyte proliferation in the duodenum, jejunum, ileum, caecum, ascending, transverse and descending colon in the rat were studied by different methods of analysis of cell population kinetics (percentage-labelled mitosis curves, cumulative labelling curves, distribution of labelling index curves, etc.). The majority of proliferating cells in the small intestine are homogenous, as far as mitotic cycle mean duration (11–12 hrs) is concerned. All proliferating cells in all the zones of the colonic crypts and the bottom of the small intestine crypts are divided into subpopulations, having different mean durations of the mitotic cycle. It is suggested that, in the crypt bottom in all intestines as well as the crypt's maximum proliferation zones in most of the colonie segments, a considerable fraction of cells has a very long mitotic cycle or enters resting phase R₁ The average value of the mean durations of the mitotic cycle of all colonie enterocyte subpopulations is 18–22 hours. On the basis of the authors' findings and literature data, a model for the enterocyte life cycle is proposed, according to which the cell flux is branched during the mitotic cycle and the crypt develops from a stem enterocyte population located at its bottom.