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M Walski

Publications and source records attributed to M Walski.

At least 55 records · Page 3Linked to original sources
PubMed1993

The perivascular fibrotic reaction in rat brain in the late period after experimental clinical death. II. Precapillary vessels.

The aim of the study was to investigate the area surrounding precapillary vessels in the temporal cortex of rat-brains. The material consisted of animals that survived a 10-minute cardiac arrest and then lived on for 10 to 12 months. In the specimens that survived 10 month we observed dilatation of the pericapillary space pervaded with unidentified cells surrounded by multiple collagen fibrils. In the close vicinity of these vessels we often discerned cells participating in the process of phagocytosis. Smooth muscle cells held numerous pinocytic vesicles which contained microfibrillar material. Collagen fibrils were also discerned beneath their basement membrane. In the animals that survived 12 months in many cases the spaces between blood vessel mural myocytes and brain cells were filled with numerous collagen fibrils. In some cases these fibrils formed bridge-like structures between vessel walls and surrounding nerve cells. These compartments were often accompanied by brain phagocytes, the cytoplasm of which contained single fibres or bundles of collagen located in the close proximity of the phagolysosomes. We discussed the role of myocytes, myofibroblasts and phagocytes in the production of reparative collagen following the destruction of precapillary vessels and brain continuity.

Animals↗
PubMed1992

The possible role of endothelium in prevention of rebleeding in experimental subarachnoid hemorrhage (SAH).

Experiments were performed on six male cats under nitrous oxide in oxygen anesthesia. Animals were paralysed and artificially ventilated. Subarachnoid hemorrhage (SAH) was produced by basilar artery puncture following clivectomy. After 10 minutes (3 cats) and 60 minutes (3 cats) the basilar artery was dissected and fixed for electronmicroscopic examination. Ultrastructural examinations revealed in the cytoplasm of the endothelial cells on the side of the vessel lumen, the presence of spherical or flattened cylindrical structures identified as Weibel-Palade bodies. In the endothelium of the proximal segment, 10 and 60 minutes after puncture, the number of these electron-dense bodies increased, and was higher than in the corresponding distal segment. The possible role of the Weibel-Palade bodies in SAH after-effects is discussed.

Animals↗
PubMed1992

The perivascular fibrotic reaction in rat brain in the late period after experimental clinical death. I. Capillary vessels.

In this paper we studied the pericapillary zone of the hypothalamic neurosecretory nuclei and temporal cerebral cortex of rats 6-12 months after experimentally evoked cardiac arrest of 10 minutes duration. The most significant ultrastructural findings were presence of single collagen fibrils and collagen bundles in the compartment between endothelia and pericytes, pericytes and basement membrane and also inside the phagocytic cells. In the animals that survived at least 10 months after resuscitation the capillaries filled with thrombocytes were encountered. Moreover, in the vicinity of these capillaries the dead cells and collagen bundles were observed. We interpret these findings as the evidence of the reparatory process in the border between capillaries and the surrounding brain cells. We discuss the hypothesis that the non-fibroblastic cells present in rat brain are able to synthesize collagen that leads to a process comparable with the fibrosis of parenchymal organs.

Animals↗
PubMed1991

Immunomodulators interfere with angiopathy but not vasospasm after subarachnoid haemorrhage in rabbits.

The present study deals with the effects of immunomodulators on the morphology of intracerebral arterial walls in rabbits with experimental subarachnoid haemorrhage (SAH). Immunostimulators:thymostimuline and inosine dimethylamino-isopropanol-p-acetamido-benzoate were found to aggravate the angiopathic changes, whereas immunosuppressive drugs-cyclosporine A and azathioprine appeared to prevent the damage. The authors consider the possibility of using immunosuppressive drugs in patients with ruptured intracranial aneurysms.

Animals↗
PubMed1991

Ultrastructure of phagocytizing cells of the rat hypothalamic neurosurgery nuclei in a remote period after the sustained clinical death.

Ultrastructural studies were carried out on neurosecretory nuclei taken from brains of rats which have survived for 16 weeks following clinical death of 5 or 10 min duration. The reported observations indicate that brain lesions were caused by changes due to ischemia and superimposed secondary changes resulting from the maturation of pathological processes. In animals subjected to clinical death for 5 min the observed cells in the perivascular area were integrated in the capillary wall and wrapped by the basement membrane. Sometimes they were accompanied by cells engaged in the process of phagocytosis. Phagocytizing cells were more frequently noted in the animals subjected to clinical death for 10 min and then their cytoplasmic processes were connected with the adjacent capillaries. We assume that these cells, which may represent cerebral macrophages occur by transformation of pericytes or blood derived monocytes.

Animals↗
PubMed1991

Ultrastructural alterations of pulmonary surfactant in rat lungs after inhibition of protein synthesis by puromycin.

The effects of systematically administered puromycin on the fine structure of the lung were studied. The effects varied depending on the duration of exposure and the time interval between the last injection and sacrifice. After short term exposure most surfactant had separated from the epithelial surface and profound alterations in the tubular myelin structure were seen. After moderate duration of exposure a previously undescribed multilamellar lining layer was observed which was often detached from the alveolar epithelium. Six hours after the last injection the regular tubular myelin pattern reappeared. Puromycin treatment results in inhibition of various proteins synthesized by type II epithelial cells. Inhibition of synthesis of some proteins, most probably that of glycoprotein A, causes a primary effect on the structure of surfactant. The loss of at least some of the cytoskeletal proteins in Type II epithelial cells apparently results in interference with exocytosis of lamellar body contents.

Animals↗
PubMed1991

Ultrastructural changes in the hypothalamic secretory nuclei of rats depending on the duration of clinical death.

The studies were carried out on neurosecretory nuclei of rat hypothalamus following complete circulatory arrest for 5 min (group I) and 10 min (group II). The surviving time of the animals after the experiment was 6 weeks. In group I, the ultrastructural appearance of the perikaryonic areas of the neurons indicates increased metabolic activity of these cells. Crinophagocytic bodies were noted near the Golgi apparatus. In the processes of neurons changes in the structure of the cytoskeletal elements were observed. In group II significant differences were noted, as compared with group I. They consisted in the desolation of the rough endoplasmic reticulum membranes from ribosomes, dilatation of the Golgi area cisternae, and swelling of mitochondria. In the perivascular region cells with the surface of the cytoplasmic processes membranes covered by the product of the Alcian blue reaction were noticed. In our opinion these cells may represent "cerebral macrophages". The ultrastructural changes were more pronounced in animals of group II, as compared with animals of group I.

Animals↗
PubMed1991

Studies on the hypothalamus and secretory nuclei of rat in the remote period following clinical death.

Ultrastructural studies of hypothalamic secretory nuclei were carried out on rats which survived 16 weeks after 5- or 10-min-long clinical death. Active neurosecretory cells were noted without any signs of injury. In perikaryonic area numerous polymorphic lysosomes and "nucleolus-like bodies" were observed. Attention was called to significant changes in the structure of cytoskeleton and observations were discussed in relation to biochemical data. In both groups of the studied animals neurosecretory cells with features of apoptosis were found. Apoptotic cells appeared more often in animals which survived 10-min-long clinical death. Characteristic morphological features of the process of apoptosis are shown in illustrations.

Animals↗
PubMed1989

[Electron-microscopic changes in neurosecretory nuclei of the rat hypothalamus after total ischemia in short-term clinical death].

Hypothalamic neurosecretory nuclei of rats in which short-term clinical death was experimentally induced, were examined electron-microscopically. Material for studies was taken two weeks after resuscitation of animals following 5 min cardiac and respiratory arrest. Application of aldehyde fixatives with Alcian blue as well as fixatives containing tannic acid revealed numerous additional ultrastructural features not visualized in routine electron microscopy. The obtained results are indicative that short-term cerebral ischemia in rats results in ultrastructural abnormalities in neurosecretory hypothalamic nuclei, which appear after 2 weeks survival. These are electron microscope exponents of reduced secretory function, increased number of lysosomal structures and changes in cytoskeleton organization. They are accompanied by abnormalities in axoplasm and myelin sheaths. The authors consider those structural abnormalities as exponents of delayed irreversible metabolic changes of nerve cells.

Animals↗
PubMed1987

Deposition and phagocytosis of inhaled particles in the gas exchange region of the duck, Anas platyrhynchos.

Little is known about the fate of inhaled aerosol particles in birds; even the anatomical location of phagocytic cells within the lungs has yet to be clearly demonstrated. We exposed 2 anesthetized, spontaneously breathing ducks to a non-toxic iron oxide aerosol (aerodynamic mass mean diameter = 0.18 micron; 460 mg/m3) for 1.75 h and 2 awake, resting ducks to less concentrated aerosol (38 mg/m3) for 6 h on two consecutive days. All 4 ducks were sacrificed 24 h after the end of the last exposure. Their lungs, as well as the lungs from a control duck not exposed to the aerosol, were fixed in situ by insufflation of osmium tetroxide vapor or by intravascular perfusion. Then samples of the gas exchange region were examined with a transmission electron microscope. We found iron oxide particles: trapped within the trilaminar substance that is unique to avian lungs and coats the atria and infundibula; within epithelial cells of the atria and initial portions of the infundibula; and within interstitial macrophages. Only occasionally, small amounts of particles were found in the air capillaries. We conclude that both epithelial cells and interstitial macrophages can phagocytize particles in avian lungs, and that there is some convective transport of aerosol to the atria and the initial portions of the infundibula.

Animals↗
PubMed1986

Influence of 0.02 M EDTA and 3 M KCl on surface of Hymenolepis diminuta and composition of isolated proteins.

The glycocalyx of Hymenolepis diminuta (Cestoda, Cyclophyllidea) was isolated using 0.02 M EDTA or 3 M KCl. It was shown in the electron micrographs that 0.02 M EDTA did not damage the tapeworm plasma membrane, eliminating glycocylax only, in contrast to 3 M KCl which disrupted tegument up to the basal membrane. The protein analysis of extracts and the supernatant of homogenate of the whole tapeworm strobila by polyacrylamide gel electrophoresis (PAGE) and dodecyl sulphate-polyacrylamide gel electrophoresis (SDS) electrophoresis revealed that the substance extracted with 3 M KCl was more abundant in protein fractions than the two remaining ones. The substance extracted with 0.02 EDTA, collecting the tapeworm glycocalyx possessed the smallest amount of protein fractions, however, some of them were more abundant.

Animals↗
PubMed1982

The influence of ethanol intoxication on cholinergic axon terminals in the rat brain. (Morphometric evaluation).

In view of the inhibitory influence of ethanol on synaptic transmission demonstrated by numerous authors, the present investigations were undertaken with the purpose of ascertaining the ultrastructural changes in the cholinergic axon terminals of the CNS caused by chronic ethanol intoxication. The experiments were made with 12 rats receiving ethanol according to RATCLIFFE'S model (1972) in increasing doses over a period of 1, 2 and 3 months. The studies comprised evaluation of the electronmicroscopic picture of synapses from the temporal cortex and morphometric analysis of the number of synaptic vesicles in the boutons, of the surface area of synapse cross sections and the surface area of the cross sections of mitochondria in the boutons. Morphometric analysis showed that chronic administration of ethanol to rats reduces the number of synaptic vesicles in the boutons, which may be caused by chronic excitation of neurons by ethanol. Impairment of mitochondria within the synaptic boutons was also noted, probably due to disturbances in cell respiration produced by ethanol. Polymorphism of synaptic vesicles was observed in the form of greatly enlarged ones. It may be interpreted as the morphological manifestation of the process of axon terminals degeneration. Moreover, planimetric analysis demonstrated a significantly increased surface area of synaptic bouton cross sections in all experimental rats as compared with the control ones. The dynamics of the observed changes was not uniform. The reduction of the number of synaptic vesicles and impairment of mitochondria were most pronounced in the early phase of intoxication. In the later period in spite of increased doses and prolonged time of ethanol treatment the changes became rather less intensive, this probably being connected with the process of adaptation. Polymorphism of the synaptic vesicles became more pronounced gradually in the successive experimental groups, probably with corresponding advancing degeneration of the axon terminals. The significantly enlarged surface area of the synaptic boutons cross sections did not show any dependence on the connection of ethanol and duration of its administration.

Acetylcholine↗
PubMed1981

Ultrastructural and morphometric investigations on the mechanism of neurotransmitter release from synaptic vesicles.

The mechanism of neurotransmitter release from synaptic vesicles as the results of neuron excitation is not quite clear. It is believed, that this process may occur by way of exocytosis into the synaptic cleft directly from the cytosol to the cleft. Ultrastructural-morphometric analysis was attempted of the synaptic vesicles from the motor cortex of mice. As stimulation model an audiogenic epileptic seizure was used. The method of ZIO impregnation was applied, which according to Kawana (7) allowed to visualise the presence of a neurotransmitter in synaptic vesicles. Morphometric analysis consisted in counting the synaptic vesicles ZIO-positive, filled with neurotransmitter, and ZIO-negative, empty ones, in 3 successive zones of the synaptic bouton in the initial and end phases of seizures. As the result of excitation the number of ZIO-positive-synaptic vesicles diminished significantly whereas the number of ZIO-negative ones did not increase proportionally. This indicates that the "dark" vesicles do not change into the "clear" ones, but they disappear completely. The applied method did not allow us to precisely establish vesicle translocation toward the synaptic cleft. Nevertheless the considerable reduction of their number with the percentual distribution of vesicles remaining the same within the particular zones of bouton, may indicate, under the assumption of translocation of vesicles, that they disappear close to the cleft, probably by way of exocytosis.

Animals↗