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Biomedical subjects

A Kapuściński

Publications and source records attributed to A Kapuściński.

At least 19 recordsLinked to original sources
PubMed1996

Blood-brain barrier methionine transport after resuscitation from 10-min cardiac arrest in rats.

In adult rats 10-min cardiac arrest was induced by the intracarotid compression of the heart vessel bundle. The animals were sacrificed at 2 weeks and 1, 2, 3 months after resuscitation. Decapitation was performed 15 sec after intracarotid injection of mixture of L-[methyl-3H]methionine (MET) and 4-iodo[n-methyl-14C]antipyrine. By means of the dual label method the brain uptake index (BUI) of amino acid (AA) in the cerebral hemisphere was calculated. MET BUI was corrected for residual vascular radioactivity after injection of [14C]sucrose. The significant increase of MET BUI was observed 1 and 2 months after resuscitation, reaching approximately 2-fold of control values. Two weeks and 3 months after resuscitation values did not differ significantly from control. The present study revealed either periodical increase of BBB permeability for MET or increased transport of AA according to metabolic needs during the postischemic reparative processes.

Animals↗
PubMed1995

Blood-brain barrier after resuscitation from 10-min clinical death in rats.

In rats 10-min clinical death was induced by intrathoracic compression of the cardiac vessel bundle. The animals were sacrificed from 15 min to 7 days after resuscitation. They were decapitated 15 sec after intracarotid injection of mixture of L-[U-14C]glutamic acid and tritiated water. Using by the dual label method the brain uptake index (BUI) and percent of injected dose of amino acid in the cerebral hemisphere were calculated. In 45% of animals an increase of amino acid transfer and rise of BUI revealed the blood-brain barrier (BBB) alterations. The most pronounced changes developed after 120 min and 1 day after resuscitation. The impaired vs. normal BBB state depends probably on uneven recovery of cerebral circulation in individual animals after resuscitation.

Animals↗
PubMed1995

Uptake of phenylalanine by the rat brain after resuscitation from cardiac arrest.

In 47 adult rats 10-min cardiac arrest was induced by the intrathoracic compression of the heart vessel bundle. The animals were sacrificed at 15, 30, 60, 120 min and 6 h or 1, 3, 7 days after resuscitation. Decapitation was performed 15 sec after intracarotid injection of mixture of L-[U-14C] phenylalanine (PHE) and tritiated water in PBS buffer. By the dual label method the brain uptake index (BUI) and percent of injected dose of amino acid in the cerebral hemisphere were calculated. A decrease of PHE uptake and drop of BUI revealed the blood-brain barrier (BBB) alterations resulting in diminution of amino acid transport into brain. The most pronounced changes developed between 15 and 120 min after resuscitation and also after 7 days. The above data revealed the decreased active transport of PHE in the early and late periods after ischemic insult.

Animals↗
PubMed1994

Increase of the brain uptake index for L-ornithine in rats with hepatic encephalopathy.

We measured the brain uptake index (BUI) for radiolabelled L-ornithine (ORN) in rats with acute hepatic encephalopathy (HE) induced by two (onset stage) or three (comatous stage) administrations of a hepatotoxin-thioacetamide (TAA). In the comatose group, an increase of the BUI to 275% of control was measured at 24 h post-treatment. In the onset group, the BUI for ORN increased gradually with time: it reached 220% of control at 7 days post-treatment and 442% of control at 21 days post-treatment. HE did not raise the BUI for a blood-brain barrier (BBB) non-penetrable amino acid L-aspartate (ASP), indicating that HE activates ORN transport but does not produce BBB leakage. ORN transport through BBB was not increased in rats with hyperammonemia comparable to that accompanying HE, but was induced without liver damage. Considering recent evidence that ORN acting intracerebrally ameliorates pathophysiological symptoms of HE, increased transport ORN across BBB should facilitate HE therapy based on systemic administration of this amino acid.

Acetates↗
PubMed1994

Atrial natriuretic peptide in the rat brain and plasma during clinical death and after resuscitation.

By means of the radioimmunologic method changes of ANP content in the rat brain and plasma have been evaluated during 5-min clinical death and up to 2 hr after resuscitation. Ischemia did not produce significant rise of ANP immunoreactivity in the brain, however, in the early postresuscitation period its reversible increase was noted with the peak value at 15th min. The content of peptide in plasma significantly increased at the end of clinical death and 5 min after resuscitation. The obtained results can support the notion of quantitative relationship between concentration of ANP and cGMP content in the brain in vivo.

Animals↗
PubMed1994

Leukotriene C4 in the rat brain after resuscitation from clinical death.

By means of the radioimmunological method changes of concentration of leukotriene C4 (LTC4) in rat brain cortex and hippocampus have been evaluated during 5-min clinical death and up to 2 h after resuscitation. Wet weight/dry weight methodology was utilized to evaluate brain water content. Ischemia did not produce significant changes of LTC4 concentration in the brain. In the postresuscitation period concentration of LTC4 in both brain regions significantly increased reaching in 5 and 15 min respectively a 4- and 5-fold control values. Later the concentration of LTC4 in the brain decreased reaching in 30 min a 3-fold control level, and in 60 and 120 min after resuscitation control values. Water content after resuscitation did not show significant changes in both brain regions. LTC4 does not seem to play an important role in the development of cerebral edema.

Animals↗
PubMed1993

Cyclic GMP levels in the rat brain and plasma during clinical death and after resuscitation.

Changes of cGMP content in the rat brain and plasma have been evaluated by means of the radioimmunologic method after 5-min clinical death and up to 2 hours after resuscitation. Ischemia produced a decrease of cGMP in the brain, however, at the 15th min after resuscitation a reversible significant rise of nucleotide concentration was noted. In plasma at the end of ischemia and in the postischemic period a significant decrease of cGMP level was observed. The mechanisms of cGMP regulation in the central nervous system and the significance of the obtained results are discussed.

Animals↗
PubMed1993

Effect of clinical death on inositol 1,4,5-trisphosphate in the rat brain.

Changes of inositol 1,4,5-trisphosphate content in the rat brain have been evaluated by means of the radioimmunologic method during 5-min clinical death and up to 2 hrs after resuscitation. Ischemia produced a decrease of IP3 content in the brain on the average to 63% of the control values. IP3 concentration in the brain increased on the average to 197% of the control values at the 15th min after resuscitation, and decreased to 127% at the 60 min. Two hours after resuscitation the IP3 content in the brain again increased on the average to 187%. The new data on brain metabolism in the ischemic conditions and the role of IP3 as the second messenger and mediator of neuromodulation processes are discussed.

Animals↗
PubMed1992

Changes in endogenous prostacyclin in the rat brain during clinical death and after resuscitation.

By means of the radioimmunologic method changes of concentration of 6-keto-prostaglandin F1 alpha (PGF1 alpha)--the stable metabolite of prostacyclin in the rat brain have been evaluated during 5-min clinical death and up to 2 hrs after resuscitation. Ischemia did not produce significant changes of 6-keto-PGF1 alpha concentration in the brain. In the early postresuscitation period the concentration of 6-keto-PGF1 in the and 7-fold control values. Later the concentration of 6-keto-PGF1 alpha in the brain decreased reaching in 30 min a 3-fold the control level, and in 60 and 120 min after resuscitation control values. The reasons of unsuccessful therapy of ischemic stroke with prostacyclin are discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Changes of concentration of cyclic AMP in rat brain and plasma in the clinical death model.

In the experimental model of clinical death in rats (Korpachev et al. 1982) cyclic AMP concentrations were evaluated in the brain and plasma at the end of 5-min clinical death, and 5, 15, 30, 60 and 120 min after resuscitation. The cAMP 125I assay system has been used. At the end of clinical death the cAMP level decreased in the brain with normalization 15 min after resuscitation; the second decrease of the cAMP level was observed 30 min post resuscitation with normalization in later periods. In the plasma cAMP concentration did not change at the end of clinical death, followed by a significant increase 5 min after resuscitation. Later the level of plasma cAMP decreased being still above the control value after 2 hours. The possible role of endogenous catecholamines stimulation on adenylate cyclase activity is discussed.

Animals↗
PubMed1989

Rapid decrease of high affinity ouabain binding sites in hippocampal CA1 region following short-term global cerebral ischemia in rat.

High affinity [3H]ouabain binding was examined in the hippocampal CA1 region and frontal cortex of rats subjected to 5 min complete cerebral ischemia in a clinical death model, and to subsequent resuscitation. A decrease of Bmax directly after ischemia and its further gradual decrease during 120 min of reperfusion were noted in the ischemia-vulnerable CA1 region, whereas no change of Bmax was observed in frontal cortex. The apparent Kd constant showed insignificant fluctuations in either of the two brain regions. Since ouabain binds with high affinity to the neuronal (alpha +)-form of Na+/K+-ATPase, the results indicate a rapid enzyme loss in CA1 neurons. The high affinity ouabain binding test proved to be a sensitive detector of premorphological changes in nerve cell membranes in ischemia.

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