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P Piotrowski

Publications and source records attributed to P Piotrowski.

At least 19 recordsLinked to original sources
PubMed2001

Neuronal death in the rat hippocampus in experimental diabetes and cerebral ischaemia treated with antioxidants.

Male Wistar rats were subjected to intraperitoneal (i.p.) streptozotocin (STZ) administration (85 mg/kg) to evoke diabetes. Cerebral ischaemia was produced by injection of 0.03 ml of air into the left carotid followed by bilateral common carotid ligation. We studied the effect of application of two antioxidants--coenzyme Q10 (CoQ10, 10 mg/kg b.w., i.p. for seven days) and lipoic acid (LA, 100 mg/kg b.w., i.p. for seven days) on neurones and on the apoptosis-related enzyme--caspase-3 activity in the hippocampus and dentate gyrus. Ischaemia and diabetes lead to a decrease of nuclear and perikaryon diameters as well as neuronal density in the CA1, CA2, CA3 and dentate gyrus. Application of CoQ10 or LA for seven days improved the mean nucleus area and perikaryon area in almost all investigated structures. Both antioxidants diminished neuronal loss in the diabetes complicated with ischaemia but not in the animals with diabetes only. Activity of one of the key enzymes in apoptotic cell death, caspase-3 (CPP32), increased in hippocampus in the diabetic rats, in the animals with cerebral ischaemia and in the rats with both diabetes and ischaemia by about 80%, 33% and 53%, respectively. Either the CoQ10 or the LA treatment led to a significant decrease of the CPP32 activity in all experimental groups. Our results confirm the presence of neuronal damage and death in the hippocampus and dentate gyrus in the experimental STZ-diabetes and its aggravation by the additional cerebral ischaemia. The effects of the antioxidative treatment support the hypothesis of an important role of oxidative stress and free radicals in neuronal pathology in diabetes and ischaemia. The above results of CPP32 activity suggest an important role of apoptosis as a mechanism of cell death and demonstrate the positive effect of the CoQ10 and the LA treatment.

Animals↗
PubMed1999

The experimental squalene encephaloneuropathy in the rat.

Accumulation of squalene in the CNS is observed after administration of tellurium and squalene has been proposed to be a mediator of tellurium encephaloneuropathy. The aim of this study was to investigate the effects of squalene on the central and peripheral nervous systems in rat at the ultrastructural level. Squalene was administered at a dose of 20 g/kg body weight, once daily for 4 days, and the animals were sacrificed 7 days and 30 days after the initiation of the experiment. After 7 days a mild swelling of mitochondria and dilation of the Golgi complex cisterns in few neurons in the cerebral cortex and hippocampus were observed. The swelling of astrocytes and their processes was also seen. Some myelin sheaths in the cerebral white matter were disintegrated. In the peripheral nervous system (the sciatic nerve), a damage of the Schwann cells, a destruction of the myelin sheaths, and lipid-like deposits between myelin lamellae causing a secondary compression of axons were present. Squalene administration caused a stimulation of fibroblast to synthesize collagen and an activation of macrophages in the perineurium. After 30 days, the lipid-like material was present in some neurons as well as in the myelin sheaths in the central nervous system. Endothelial cells were hypertrophic and a few demonstrated features of apoptosis. Endothelial cell hypertrophy caused a narrowing of vessel lumen associated with an aggregation of blood morphological elements. Disturbances in myelination and swelling of astrocytic processes persisted in the central nervous system. In the peripheral nervous system, lipid-like deposits were localized in some fibroblasts and extracellularly between the collagen fibers in the perineurium. In conclusion, our electron microscopic studies indicate that squalene produces characteristic pathological changes both in the central and peripheral nervous systems. However, these alterations differ in some aspects (changes in endothelia, accumulation of lipid-like material) from the known features of tellurium encephaloneuropathy.

Animals↗
PubMed1999

Morphology of experimental diabetes and cerebral ischemia in the rat brain.

Male Wistar rats were subjected to streptozotocin administration (85 mg/kg i.p.) and to cerebral air embolia with common carotids ligation. Light microscopy studies showed foci of neuronal loss and dark neurons especially in hippocampus, dentate gyrus, amygdaloid, thalamus and hypothalamus in the diabetic rats. Cerebral ischemia aggravated above changes and additionally, small hemorrhagic foci in putamen close to globus pallidus were observed. Our results indicate on chronic, generalized pathologic process in diabetic-rat's brain, which may be related to an oxidative stress and leads to a death of neurons in necrotic or apoptotic way.

Amygdala↗
PubMed1999

Electron microscopy studies on experimental diabetes and cerebral ischemia in the rat brain.

Male Wistar rats were subjected to streptozotocin administration (85 mg/kg i.p.) and to cerebral air embolia with common carotids ligation. Electron microscope studies showed dark neurons, degeneration of endothelial cells and changes in basement membrane of brain capillaries, and changed astroglia in diabetic rats. Our results seem to support our previous findings in light microscopy and correspond with some others authors' suggestions that diabetes leads to chronic, generalized pathologic process in diabetic-rat brain, not-only dependent on vascular pathology, but which may be related to an oxidative/metabolic stress leading to a death of neurons in necrotic or apoptotic way.

Amygdala↗
PubMed1998

Evaluation of morphological changes after treatment with coenzyme Q10 (CoQ10) in endothelin-1 induced experimental ischemia in the rat.

The aim of the work was to evaluate the effect of CoQ10 (10 mg/kg body weight) on the morphological changes in the rat brain after the Et-1 induced cerebral ischemia. Selective necrotic foci and dark neurons were observed in the cerebral cortex, hippocampal CA1, CA2 sectors and dentate gyrus after the administration of Et-1. Around the necrotic foci, glycogen was deposited 24 hours after the ischemic hypoxia. It seems that histopathological changes evoked by Et-1 indicate the complicated mechanism connected with ischemia. After treatment with CoQ10 only sparse neuronal changes were observed. CoQ10, known oxygen-derived free radicals scavenger diminished neuronal damage in the cerebral cortex and in the hippocampus.

Animals↗
PubMed1997

Experimental squalene encephaloneuropathy in the rat.

To investigate the influence of squalene on the nervous system, adult male Wistar rats were injected with squalene subcutaneously with 20 g/kg of the body weight for 4 consecutive days. After 7 or 30 days from the initiation of the experiment, brain and ischiadic nerves were harvested for electron microscopy. Squalene affected mostly PNS targeting Schwann cells and myelin sheaths. Accumulation of lipid-like droplets in the myelin sheaths in the PNS and in the neurons in the brain cortex, hypertrophy of endothelium, and sometimes endothelial apoptosis in blood vessels, and increased synthesis of collagen in the ischiadic nerve were characteristic for developed squalene encephaloneuropathy.

Animals↗
PubMed1996

Maternal cells are widely distributed in murine fetuses in utero.

Passage of maternal cells into conceptuses in utero is recognized but poorly defined in species with hemochorial placentation. Despite the potential importance for such a phenomenon in vertical disease transmission, only limited data address the frequency of material to fetal cell trafficking or the developmental stage of its initiation. A murine model system, involving transfer of LacZ-, scid/scid, or wild type (+/+) blastocysts to pseudo-pregnant, LacZ+ transgenic ROSA26 females provided both flow cytometric and in situ information. In 100% of the late-gestation pregnancies studied, nucleated LacZ+ maternal cells crossed to conceptuses. In 90% of scid/scid fetuses, nucleated maternal cells were present in at least one lymphoid organ and often in more than one organ. Thymus was the most frequent site for maternal cell detection while the highest proportions of maternal cells were found in liver. Maternal cells were also visualized in fetal lung, heart, and bone marrow. Maternal cell trafficking into scid/scid fetuses commenced about midgestation, coincident with maturation of a placental circulation. In late-gestation +/+ fetuses, maternal cells were found extensively throughout bone marrow but not in other organs. The presence of maternal cells within primary lymphoid organs of fetuses may influence the repertoire of the developing fetal immune system and may be an underappreciated mechanism for vertical disease transmission.

Animals↗
PubMedDate not supplied

[Effect of hypothermia on lactate acidosis in experimental ischemia of rat brain].

The aim of the work was to evaluate the effect of hypothermia on lactate level in the rat cerebral ischaemia. Adult male Wistar rats were subjected to injection of 0.05 ml of air into the ligation of left common carotid artery. Lactate level increased in cerebral hemispheres after 4 hours following air emboli. Mild hypothermia (28 degrees-31 degrees C) continued for 4 hours of cerebral ischaemia, and its beneficial effect was observed. A statistically significant decrease of lactate concentration was noted. The above phenomenon was confirmed by the increase of cerebral acidosis after 24 hours when mild hypothermia was interrupted from the 4th hour of the experiment on. It seems to be of a great importance to adjust proper time of initiation and a duration of hypothermia in cerebral ischaemia treatment.

Acidosis, Lactic↗
PubMedDate not supplied

[The effect of coenzyme Q10 on lactate acidosis at the beginning of experimental cerebral ischemia in rats after the use of endothelin 1 (preliminary results)].

The aim of the work was to evaluate effect of CoQ10 on the lactate level in the rat brain after administration of Et-1. Fifty-three male Wistar rats (approximately 220-250 g) were used in the experiment. The animals were divided into four groups. 1. control; 2-4 under chloride hydrate anaesthesia, the rats were subjected to stereotaxic injection into right cerebral lateral ventricle: 2. 1 microliter Ringer's solution (control) and i.p. 0.5 ml of soybean oil, 3. 10 pmoles Et-1 diluted in 1 microliter Ringer's solution and i.p. 0.5 ml soybean oil, 4. 10 pmoles Et-1 diluted in 1 microliter Ringer's solution and i.p. 10 mg/kg of the body weight CoQ1O (Sigma). Right and left hemispheres were taken after one hour, 4 and 24 hours and the lactate level was assayed by an enzymatic method. Et-1 evoked a significant increase of lactate level at all experimental time intervals. CoQ10 reduced lactate acidosis after 24 hours from the administration of Et-1. The above phenomenon can be explained among other by an improvement of the cellular respiratory activity. CoQ10 represents very important electron transporter from flavins to cytochromes in the respiratory chain. Therefore CoQ10 can be used for prevention and treatment of ischaemic insult in human cases.

Acidosis, Lactic↗