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Biomedical subjects

M Walski

Publications and source records attributed to M Walski.

At least 37 records · Page 2Linked to original sources
PubMed1999

Changes in the extracellular profiles of neuroactive amino acids in the rat striatum at the asymptomatic stage of hepatic failure.

Rats were treated with a hepatotoxin thioacetamide (TAA) and examined 21 days later, when they showed moderate fatty metamorphosis of the liver and morphological changes in brain indicative of excitotoxic neuronal damage, but no evident biochemical or neurophysiological symptoms of hepatic encephalopathy (HE). High-performance liquid chromatography (HPLC) analysis of extracellular amino acids in striatal microdialysates of TAA-treated rats revealed a significant increase in the excitatory amino acids glutamate (Glu) and aspartate (Asp) and their amino acid metabolites glutamine (Gln) and alanine (Ala). Microdialysis in the presence of 50 mM K+ triggered in TAA-treated rats an accumulation of Asp and Glu, and diminished the accumulation of Gln. These effects were virtually absent in control rats. None of the treatments affected the accumulation of the nontransmitter amino acid leucine (Leu). The above changes mirror those previously described in symptomatic HE and are likely to contribute to excitotoxic damage. The basal microdialysate content of taurine (Tau), an amino acid with antioxidant and volume regulatory properties, was 60% lower in TAA-treated rats than in control rats despite its increased blood-to-brain transport. The decrease in extracellular Tau may thus reflect Tau redistribution to adjacent central nervous system (CNS) cells manifesting a cell-protective response. Stimulation with 50 mM K+ increased extracellular Tau in control rats by 182% and in TAA-treated rats by 322%. Stimulation with 100 microM N-methyl-D-aspartate (NMDA) increased extracellular Tau in control rats by 27 % and in TAA-treated rats by as much as 250%. The increase of K+- or NMDA-dependent Tau release may reflect improved cell volume regulation and neuroprotection and contribute to attenuation of neurologic symptoms in rats with liver failure.

Alanine↗
PubMed1999

Light and electron microscopic picture of atherosclerotic plaque in stable and unstable angina.

By presenting this series of 127 cases of coronary atherectomy the authors join the workers who study morphological differences between the atherosclerotic plaques in stable and unstable angina. Routine staining of formalin-fixed, paraffin-embedded material was completed by the detection of T lymphocytes, macrophages, mast cells, smooth myocytes and grown-in capillaries using monoclonal antibodies (DAKO), as well as by the immunofluorescent demonstration of fibrinogen in the plaques. The plaques derived from patients with unstable angina showed a higher incidence of mast cells (significant) and macrophages (insignificant). These cells render the plaque more susceptible to rupture or fissuring. There was also significantly more frequent and quantitatively more abundant permeation of the plaque by fibrinogen that raises the chance of thrombosis. These findings support the view that unstable angina correlates with the phenomena that favour the rupture of the plaque and thrombosis. Electron microscopy has not been used so far to study coronary atherosclerotic plaques. This material includes 15 plaques from stable and 18 plaques from unstable angina. A cover of fibrin and blood platelets is a regular formation on the surface and in the superficial layer of the plaque from unstable angina. It contributes to the "thrombotic proneness" of the coronary artery. These plaques also show abundant elastic fibres. This pattern corresponds to myo-elastic intimal hyperplasia ("intimal thickening") where the production of intimal elastin constitutes an essential phenomenon. Intimal thickening is interpreted as a preatherosclerotic event. The presence of elastin reflects an early stage of the development of the plaque. The plaque from stable angina shows abundant collagen fibres, which aggravate the lesion.

Adult↗
PubMed1999

Electron microscopic studies on NO-synthase activity in brain phagocytes of rat cerebral cortex after ischemic and traumatic brain injury.

In the present study we used a cytochemical method for electron microscopy for nitric oxide synthase (NOS) detection in rat cerebral cortex. The animals were subjected to total brain ischemia and mechanical trauma. Tissue was fixed in 3% paraformaldehyde and 0.5% glutaraldehyde which enabled excellent preservation of cellular ultrastructure and resulted in an increase in method reproducibility. The results show the distribution of the particles reflecting the sites of NOS activity in the capillaries and other, more distant locations. NOS activity was found in thrombocytes, endothelium and pericytes. Moreover, the morphologically differentiated perivascular phagocytes demonstrated NOS reaction product in their cytoplasm. These phagocytes containing polymorphic phagolysosomes, surrounded the fragments of damaged neurons. We propose that these cells are descendants of blood-borne monocytes and transformed pericytes. In the areas distant to the sites of injury we noticed cells showing ultrastructural features of activated microglia. These cells were in a close contact with neural perikarya and contained iNOS-specific reaction product in the cytoplasm. In conclusion, our studies revealed differentiated forms of brain phagocytes, the occurrence of which depended on the type of cerebral injury. These cells demonstrated NOS reaction product suggesting their role in cerebral NO production during ischemia and other forms of brain injury.

Animals↗
PubMed1998

The application of microspheres from the copolymers of lactide and epsilon-caprolactone to the controlled release of steroids.

The microspheres made of the copolymers of lactide and epsilon-caprolactone were used for the controlled release of progesterone and beta-estradiol. The copolymers contained 83-94% of l or d,l-lactide. The influence of the microstructure of lactidyl blocks in the copolymer chains on the drug release rate was studied. More uniform release rate was observed in the case of the copolymer derived from d,l-lactide as composed to l-lactide. For the copolymer containing 83-94% of d,l-lactide units the progesterone and beta-estradiol release rate in vitro was found to be practically constant within over 40 days. The in vivo studies performed on rats revealed that the period of constant release rate of beta-estradiol can be prolonged to about 70 days. The microspheres made of the applied poly-(d,l-lactide-co-epsilon-caprolactone) are the convenient system for long time release of steroids.

Animals↗
PubMed1998

Retinal gliopathy accompanying thioacetamide-induced liver insufficiency: light and electron microscopic observations.

A recent examination of retinae of patients who had died with symptoms of liver insufficiency (LI) including hepatic encephalopathy (HE) revealed morphological changes in retinal Müller glia similar to the astrocytic changes normally accompanying HE, and the term "hepatic retinopathy" (HR) was coined to define these changes. In the present study, the immunomorphology and ultrastructure of Müller cells were examined in rats in which LI with accompanying HE was induced with a hepatotoxin, thioacetamide (TAA). Light microscopically, retinae of rats with LI were characterized by swelling of the Muller cell cytoplasm. Immunostaining for glia-specific marker proteins in Müller cells from LI rats revealed a strongly enhanced expression of glial fibrillary acidic protein, and a considerable increase in glutamine synthetase immunoreactivity, as compared to control animals. Ultrastructurally, the Müller cells of LI rats showed swelling and vacuolization of cell processes. In particular, the endfeet contained many swollen mitochondria. By contrast, LI produced no morphologically demonstrable changes in retinal neurons and photoreceptor cells. Thus, the retinal changes induced by TAA in the rats strongly resembled those described in human HR, rendering the present rat model suitable for more detailed investigations of the pathomechanism(s) of HR.

Animals↗
PubMed1998

Arachidonate transport through the blood-retina and blood-brain barrier of the rat after reperfusion of varying duration following complete cerebral ischemia.

The permeability-surface area product (PS) of [1-14C]arachidonate at the blood-retina and blood-brain barrier was determined by short carotid perfusion in young Wistar rats 1 or 6 h after recovery period following complete cerebral ischemia induced by temporary cardiac arrest. For the retina and structures of visual system, hypothalamus and olfactory bulb there was no significant difference over sham-operated rats among mean PSs. For cortex, hippocampus and striatum, significant increases were found at both time intervals of recovery after cardiac arrest. The ischemia-reperfusion model was characterized by a significant increase in tissue conjugated diene in the hippocampus and microsomal lysophosphatidylcholine acyltransferase activity in the cortex. Consistent with these findings, we also show ultrastructural evidence mainly represented by partial opening of interendothelial junctions and mild signs of tissue edema in surrounding neuropil, suggesting barrier leakiness predominantly in the cortex, hippocampus and striatum but almost absent in the retina microvessels. Our results indicate that ischemia-reperfusion does affect influex through blood-brain barrier into regional structures of rat central nervous system of arachidonate, a metabolic substrate and lipid mediator rapidly incorporated into microcapillary and brain lipids. The data also suggested that: (i) reactive oxyradicals were moderately generated during the early phase of ischemic-reperfusion process in the rat; (ii) after reperfusion, in vitro susceptibility of different brain regions to iron-induced peroxidation was highest in the hippocampus and lowest in the cortex and striatum; (iii) membrane phospholipid repair mechanisms were activated at the same time.

Acyltransferases↗
PubMed1998

Ultrastructural localization of thiamine pyrophosphatase in plasma membranes of brain phagocytes long time after cardiac arrest.

Brain phagocytes are members of a heterogeneous family of microglial cells. In this study we investigated the membrane activity of the enzyme, thiamine pyrophosphatase (TPP-ase), in brain phagocytes. Studies were performed on rats subjected to a transient ischemia because ischemic incident precipitates proliferation of microglial cells in the brain. Brain tissue was sampled from animals that survived 12 months after experimentally evoked cardiac arrest. The product characteristic for TPP-ase activity was present in the Golgi cisterns of neurons, basement membranes of endothelia and capillary pericytes. TPP-ase activity was present on plasma membranes of brain phagocytes. The phagocyte TPP-ase activity did not depend on the anatomical localization of the cell in the brain (cortex, hippocampus, hypothalamus). Thus, TPP-ase activity can be considered as a marker of brain phagocytes.

Animals↗
PubMed1998

Characterization of thiamine pyrophosphatase positive phagocytic cells in the neural lobe of rat pituitary.

Here, using a histochemical staining for a microglia/phagocyte marker TPP-ase (Murabe, Sano 1981), and an electron microscopy we characterized the population of pituitary phagocytic cells activated by cerebral ischemia. An intense thiamine pyrophosphatase (TPP-ase) activity was demonstrated in glial cells and some cells of blood vessels of neural lobe, late period (12 months) after experimental ischemia. TPP-ase positive cells were ultrastructurally identified as pituicytes, microglia, pericytes and perivascular cells. The product characteristic for TPP-ase activity was seen on plasma membrane of these cells. Our electron-microscopic histochemical results provide strong support for a role of pituicytes, pericytes and perivascular cells as a phagocytic cells involved in mechanism of elimination of ischemically damaged axonal endings in neural lobe.

Animals↗
PubMed1997

Lead-induced abnormalities in blood-brain barrier permeability in experimental chronic toxicity.

The aim of this paper was to determine whether prolonged drinking of lead acetate-containing water by adult rats, which imitates environmental exposure to lead (Pb), affects some morphological and biochemical properties of rat brain microvessels. We noted a significant increase of lead level in capillaries and synaptosomes obtained from brains of rats under chronic toxicity conditions. Intravenously injected horseradish peroxidase (HRP) was used to evaluate the functional state of the blood-brain barrier (BBB). The results indicate that, systematically administered at low doses, lead induces BBB dysfunction. The changes, revealed in light microscopy and confirmed by electron microscopic studies, are typical for "leaky" microvessels, reported for variety of neuropathological conditions associated with BBB damage. Enhanced pinocytotic activity of the endothelial cells and the opening of interendothelial tight junctions, together with enormous phagocytizing action of the pericytes, are the most characteristic ultrastructural features noted. The presence of specific type of perivascular cells containing droplets of lipids in the cytoplasm, together with changes in phospholipid profile in brain capillaries, suggest that altered lipid composition of membranes may, at least in part, be responsible for changes in observed membrane permeability.

Animals↗
PubMed1997

Ultrastructural manifestation of pharmacologic inhibition of the activities of lipases and proteases in the cat carotid body.

This study is based on the premise that if a subcellular element of an organ performs an appreciable functional role, then its inhibition could influence the ultrastructural organization of the organ. We addressed this issue in the investigation on the carotid body, a chemosensory organ, by comparing the ultrastructure of its parenchyma in phenylmethylsulfonyl fluoride (PMSF)-injected cat with that of the normal cat. PMSF, an inhibitor of lipases and proteases, induced degenerative changes chiefly in subcellular components other than the neurosecretory and synaptic elements being associated with signal transduction. The study suggests that the inhibited enzymes might also have to do with the carotid body function.

Animals↗
PubMed1995

Crystalloid structures in the neuronal nuclei of the cerebral cortex of rats following total ischaemia.

The study was concerned with the nuclei of neurons derived from the cerebral cortex of rats that underwent experimental cardiac arrest for a duration of 10 minutes and then, after reanimation, survived from 2 weeks up to 10 months. The animals were divided into two groups: in the first-those specimens that survived from 2 to 6 weeks; in the second-those that survived 8 weeks to 10 months. In the specimens obtained from the first group we observed irregular vesicular structures and bundles of parallel fibrils 8 nm in diameter. In the second group we often observed paracrystalline form resembling "plaited ropes" and tubulous structures linked by a microfibrillar netting. These structures were analysed with a gonyometer. We believe that both the paracrystalline and the irregular vesicular structures that have been observed in the neurons obtained from ischaemic brains appeared due to the alterations in the structure of the karyoskeleton and that the observed intracellular structures are not specific for post-ischaemic alterations.

Animals↗
PubMed1995

Brain phagocytes and the microglia of the cerebral cortex of rats following an incident of total ischaemia.

The aim of the study was to point out the presence of phagocytes and active microglial cells in the cerebral cortex of rats that survived from 6 weeks to 12 months after clinical death. The number of perivascular phagocytes increased with the period of time survived after reanimation. These cells were found to be multipotential, they participated in the enzymatic degradation of cellular elements damaged in the course of clinical death. In areas distant from the capillary vessels the presence of many forms of microglial cells was revealed. The majority of them belonged the dendrous microglia. Their numerous cytoplasmic processes proved their ability to migrate. The results of the study show an increase of pathological processes in the brain, which is proportional to the length of time survival after reperfusion following cardiac arrest. The main participants in this process are the perivascular phagocytes and active cells of the dendrous microglia.

Animals↗
PubMed1994

Ammonia added in vitro, but not moderate hyperammonemia in vivo, stimulates glutamate uptake and H(+)-ATPase activity in synaptic vesicles of the rat brain.

The uptake of radiolabelled neurotransmitters: glutamate (GLU), GABA, and dopamine (DA) and the activity of the vacuolar type H(+)-pumping ATPase (H(+)-ATPase), were measured in crude synaptic vesicles treated in vitro with a neurotoxic (3 mM) dose of NH4+ (acetate or chloride), or isolated from rats with a moderate increase of brain ammonia (to approximately 0.6 mM) induced by i.p. administration of ammonium acetate (HA rats) or a hepatotoxin-thioacetamide (HE rats). In vitro treatment with ammonium salts increased the sodium-independent, chloride-dependent uptake of GLU but did not stimulate the uptake of GABA or DA. The in vitro treatment also stimulated the H(+)-ATPase activity. Since H(+)-ATPase generates the electrochemical gradient driving synaptic vesicular neurotransmitter transport, its stimulation by ammonia may have facilitated GLU uptake. However the GLU specificity of the effect must be related to other factors differentially affecting GLU uptake and the uptake of other neurotransmitters. Enhanced GLU accumulation in the synaptic vesicles may contribute to the increase of synaptic GLU exocytosis previously reported to accompany acute increases of brain ammonia to toxic levels. However, GLU uptake and H(+)-ATPase activity, but also the uptake of GABA and DA, were unchanged in synaptic vesicles prepared from rats with HA or HE. This indicates that changes in GLU and/or GABA release reported for moderate hyperammonemic conditions must be elicited by factors unrelated to the synaptic vesicular transport of the amino acids.

Ammonia↗
PubMed1994

Lead as an inductor of some morphological and functional changes in synaptosomes from rat brain.

1. The effect of lead (in vivo) on the uptake of GABA, dopamine, and histidine as a precursor of histamine in synaptosomes obtained from chronically lead-treated rats was studied. 2. Lead decreased the uptake of GABA, increased the uptake of dopamine, and did not change the uptake of histidine. These effects were independent of calcium concentration. 3. Lead administration to the rat changed the morphology of the synaptosomes, as manifested in the decreased number of synaptic vesicles and disturbed mitochondrial structure. 4. The results suggest the existence of several mechanisms of lead toxicity on uptake, related to individual neurotransmitters, which are not necessarily connected with a Pb2+/Ca2+ interaction.

Animals↗
PubMed1994

Platelet occlusion phenomenon after short- and long-term survival following complete cerebral ischemia in rats produced by cardiac arrest.

Platelet interaction with cerebral microvessels was studied in rats after global brain ischemia. Studies were performed with a model of global central nervous system ischemia produced by cardiocirculatory arrest in normothermic rats. The ischemic period of 5-min was followed by times of recirculation lasting 5 and 15 mins, 1, 3, 6, 24, and 48 hrs, and 6, 10, and 12 months. After different periods of survival, blood vessels from brains were examined by transmission electron microscopy. Our investigation revealed numerous platelet aggregates of varying sizes within both arterial and venous intraparenchymal vessels. At the same time, we also noted platelets in various stages of disintegration. Platelets close to the endothelial cells were often degranulated, with shape changes including pseudopodia. Aggregates of platelets were focal, random, and more widespread occurring in the cerebral cortex, thalamus, basal ganglia, hippocampus, and cerebellum. We also observed recent aggregates of platelets and thrombi, which presented varying degrees of degranulation. In one time period, some platelets were found outside the brain vessels (in the perivascular space after 24 hrs of survival). We present evidence that platelet aggregation was repeated a long time after the ischemic incident, i.e., after one year. The main result was a prominent and local accumulation of platelets in microvessel branches or regions of vessel bifurcations, which correlated well with blood-brain barrier alterations observed previously in this model. The platelet aggregations increased in frequency with longer periods of recirculation. We noted that local platelet adhesion/aggregation was present after brain ischemia requiring no denudation or exposure of the basal lamina.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

2-Chloro-2' deoxyadenosine prevents angiopathic changes in cerebral arteries in experimental SAH in rabbits.

We compared the morphology of the basilar artery walls in rabbits with experimental subarachnoid haemorrhage (SAH) without and with concomitant treatment with a novel immunosuppressive drug, 2-chloro-2'-deoxyadenosine (2 CdA). The treatment was successful in the prevention of the angiopathic changes, most likely due to its ability to inhibit lymphocyte activation in response to mitogenic signals. Since lymphocyte (and monocyte?) activation may play an important role in the development of the delayed neurological deficits in patients following SAH, the use of 2 CdA to prevent these deficits shall be considered.

Animals↗