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Brain protein synthesis in rats with portacaval shunts

100%

Helewski K., Konecki J.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 4

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Features of pharmacotherapy of hepatic encephalopathy manifestations in liver cirrhosis

86%

Maretskyi V., Lobanets N.

Health Problems of Civilization

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2015

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tom 09

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nr 2

The aim of this work is to study the effect of drug mebikar on the clinical manifestations of hepatic encephalopathy in patients with liver cirrhosis. The study involved 34 patients with cirrhosis of different etiologies. The average age of the examined patients was (48.5±0.9) years, that prevailed patients of working age, indicating the medical and social significance of the problem of early diagnosis and adequate treatment of cirrhosis. One of the most frequent complications of cirrhosis is hepatic encephalopathy. In addition to conventional clinical and laboratory findings in patients with liver cirrhosis, severities of hepatic encephalopathy were determined according to West-Haven criteria before and after treatment. In patients with liver cirrhosis was established the presence of latent or clinically expressed hepatic encephalopathy. The treatment of the control group of patients consisted of the following drugs: essential phospholipids, mixture of sorbitol and major ions, arginine glutamate, furosemide, verospiron, lactulose, amoxicillin trihydrate and lansoprazole. In the complex treatment of the main group of patients medicine mebikar was administered additionally. Analysis of the clinical manifestations of hepatic encephalopathy showed a marked improvement in patients who received additional treatment with mebikar. Specifically, the incidences of mood changes as well as anxiety decreased in this group on average of 38% compared with those patients without an additional treatment with mebikar. Also, sleep disturbances in the main group was observed to be lower by 7.2% compared to those in the control group. Inclusion in the treatment of patients with liver cirrhosis, the drug mebikar – a daytime tranquilizer with anxiolytic properties reduces neurotic disorders, improves emotional state which may indicate a regression in the manifestations of hepatic encephalopathy thereby improving the quality of life of patients and thus substantiating an expedient inclusion of mebikar an anxiolytic drug to the complex therapy of patients with liver cirrhosis.

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High hepatotoxic dose of paracetamol produces generalized convulsions and brain damage in rats. A counteraction with the stable gastric pentadecapeptide BPC 157 (PL 14736)

72%

Ilic S., Drmic D., Zarkovic K., Kolenc D., Coric M., Brcic L., Klicek R., Radic B., Sever M., Djuzel V., Ivica M., Boban Blagaic A., Zoricic Z., Anic T., Zoricic I., Djidic S., Romic Z., Seiwerth S., Sikiric P.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 2

We focused on stable gastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, MW 1419, an anti-ulcer peptide efficient in inflammatory bowel disease trials (PL 14736), no toxicity reported) because of its hepatoprotective effects. We investigate a particular aspect of the sudden onset of encephalopathy with extreme paracetamol overdose (5 g/kg intraperitoneally) so far not reported: rapidly induced progressive hepatic encephalopathy with generalized convulsions in rats. BPC 157 therapy (10 µg, 10 ng, 10 pg/kg, intraperitoneally or intragastrically) was effective (µg-ng range) against paracetamol toxicity, given in early (BPC 157 immediately after paracetamol, prophylactically) or advanced stage (BPC 157 at 3 hours after paracetamol, therapeutically). At 25 min post-paracetamol increased ALT, AST and ammonium serum values precede liver lesion while in several brain areas, significant damage became apparent, accompanied by generalized convulsions. Through the next 5 hour seizure period and thereafter, the brain damage, liver damage enzyme values and hyperammonemia increased, particularly throughout the 3-24 h post-paracetamol period. BPC 157 demonstrated clinical (no convulsions (prophylactic application) or convulsions rapidly disappeared (therapeutic effect within 25 min)), microscopical (markedly less liver and brain lesions) and biochemical (enzyme and ammonium serum levels decreased) counteraction. Both, the prophylactic and therapeutic benefits (intraperitoneally and intragastrically) clearly imply BPC 157 (µg-ng range) as a highly effective paracetamol antidote even against highly advanced damaging processes induced by an extreme paracetamol over-dose.

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Electrophysiological correlates of attentional processes in patients with liver cirrhosis without minimal or clinically-overt hepatic encephalopathy

72%

Ciecko-Michalska I., Binder M., Wyczesany M., Szewczyk J., Senderecka M., Wojcik J., Dziedzic T., Slowik A., Mach T.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 4

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Cognitive evoked response potentials in patients with liver cirrhosis without diagnosis of minimal or overt hepatic encephalopathy. A pilot study

72%

Ciecko-Michalska I., Wojcik J., Wyczesany M., Binder M., Szewczyk J., Senderecka M., Dziedzic T., Slowik A., Mach T.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 3

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Rat cerebral mitochondrial glutaminase activity is unaffected by moderate hyperammonemia in two models

72%

Albrecht J., Hilgier W., Faff L.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 2

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Effect of acute hepatic encephalopathy on [3 H]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2plus

51%

Borkowska H. D., Oja S. S., Hilgier W., Saransaari P., Albrecht J.

Acta Neurobiologiae Experimentalis

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2000

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tom 60

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nr 1

Hepatic encephalopathy (HE) is characterized by motor symptoms associated with disturbed functions of the dopaminergic systems, but the underlying mechanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KC1) -stimulated release of newly loaded [3H]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2+. In the present study we compared the effects of HE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the presence and absence of Ca2+. HE enhanced the KCl-stimulated [3H]dopamine release from striatal and frontal cortical synaptosomes in the presence of Ca2+ to the same extent as in slices prepared from the respective brain regions. In the absence of Ca2+ a slight reduction in dopamine release was observed in frontal cortical synaptosomes from HE rats when compared to control rats, while no effect of HE on the release was discernible in frontal cortical and striatal slices and striatal synaptosomes. We conclude that in both brain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ influx without affecting the release mediated by means of plasma membrane transporters or exocytosis involving intraterminal Ca2+.

Ograniczanie wyników

Brain protein synthesis in rats with portacaval shunts

Features of pharmacotherapy of hepatic encephalopathy manifestations in liver cirrhosis

High hepatotoxic dose of paracetamol produces generalized convulsions and brain damage in rats. A counteraction with the stable gastric pentadecapeptide BPC 157 (PL 14736)

Electrophysiological correlates of attentional processes in patients with liver cirrhosis without minimal or clinically-overt hepatic encephalopathy

Cognitive evoked response potentials in patients with liver cirrhosis without diagnosis of minimal or overt hepatic encephalopathy. A pilot study

Rat cerebral mitochondrial glutaminase activity is unaffected by moderate hyperammonemia in two models

Effect of acute hepatic encephalopathy on [3 H]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2plus