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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The density and size of astrocyte-, oligodendrocyte- and neurone nuclei in corpus striatum were determined in rats with CCl4-induced liver encephalopathy by means of an electronic image analyzer. After 8 weeks of CCl4-administration, the astrocyte number had nearly doubled, and astrocytes with increased nuclear size appeared. After 20 weeks, a reduction (appr. 25%) was found in the number of nerve cells and oligodendrocytes. The total number of glial cells, however, was unchanged during the experiment; this demonstrates the need of performing differential counts when evaluating gliosis. Probably, a part of the increase in the number of astrocytes was due to a transformation from precursor cells, usually classified as oligodendrocytes. The increased number and size of astrocyte nuclei are probably connected with an enhanced astrocyte metabolic capacity due to alterations in the ammonia and amino acid metabolism.
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PMID:Glial and neuronal alterations in the corpus striatum of rats with CCl4-induced liver disease. A quantitative morphological study using an electronic image analyzer. 83 49

The density and size of astrocyte-, oligodendrocyte-and neurone nuclei in corpus striatum were determined in rats with CCl4-induced liver encephalopathy by means of an electronic image analyzer. After 8 weeks of CCl4-administration, the astrocyte number had nearly doubled, and astrocytes with increased nuclear size qppeared. After 20 weeks, a reduction (appr. 25 per cent) was found in the number of nerve cells and oligodendrocytes. The total number of glial cells, however, was unchanged during the experiment; this demonstrates the need of performing differential counts when evaluating gliosis. Probably, a part of the increase in the number of astrocytes was due to a transformation from precursor cells, usually classified as oligodendrocytes. The increased number and size of astrocyte nuclei are probably connected with an enhanced astrocyte metabolic capacity due to alterations in the ammonia and amino acid metabolism.
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PMID:Glial and neuronal alteration in the corpus striatum or fats with CCl4--induced liver disease. A quantitative morphological study using an electronic image analyzer. 84 80

An investigation of the mechanism of development of hepatic encephalopathy induced by CCl4 was performed in rats. CCl4 (1.0 ml/kg three times per week for over 10 weeks) caused hepatic encephalopathy in 80% of the treated rats. Accompanying the hepatic encephalopathy were hematemesis, abdominal dropsy, and hyperammonemia, conditions observed in hepatic coma patients. The blood ammonia levels were tremendously increased in only those rats with hepatic encephalopathy. Hepatic activities of carbamylphosphate synthetase (CPS) and argininosuccinate synthetase (ASS), important enzymes of the urea cycle, were significantly inhibited by CCl4. However, the causality between the inhibition of CPS or ASS activity and the increase in blood ammonia levels was not observed. On the other hand, the content of ATP, which is a substrate of CPS and ASS, was decreased by 60% in liver of rats with hepatic encephalopathy. The activity of Mg2+-ATPase which can decompose hepatic ATP was increased by 60 and 300% in mitochondria and microsomes, respectively, of livers of rats with CCl4-induced encephalopathy. There was a good correlation between the decreased hepatic ATP content and the increased mitochondrial Mg2+-ATPase activity. Furthermore, there was also a good correlation between the increase in blood ammonia levels and the increase in Mg2+-ATPase activity in microsomes. These findings suggest that hyperammonemia, which was produced by the decrease in hepatic content and by the inhibition of CPS and ASS, may play an important role in induction of hepatic encephalopathy.
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PMID:Blood ammonia levels and hepatic encephalopathy induced by CCl4 in rats. 296 38

Encephalopathy caused by hepatic cirrhosis is often associated with portasystemic shunt and hepatic parenchymal injury. Together, these are known as a combined-type symptom. Two experimental hepatic comatose models with combined-type symptom were developed in rats. Both of these models involve the administration of ammonium acetate (500 mg/kg) into the cecum in portacaval shunted (PCS) rats. In addition, hepatic injury was induced in one model by carbontetrachloride (CCl4) and in the other by dimethylnitrosamine (DMNA). These model rats showed a higher increase in the concentration of ammonia in the blood and a higher incidence of coma as determined by the loss of the righting reflex than did rats subjected to a shunt only (PCS operation + ammonia loading) or hepatic parenchymal injury only (CCl4 treatment + ammonia loading). The effect of lactitol, administered orally for 7.5 days, on the experimental hepatic coma was compared with that of lactulose. Lactitol significantly inhibited the increase in blood and brain ammonia concentration at doses of 3 and 6 g/kg/day and also reduced the incidence of coma. The effects of lactitol were similar to those of lactulose, a therapeutic agent for hepatic encephalopathy. Therefore, lactitol should be useful in the clinical treatment of hyperammonemia or hepatic encephalopathy.
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PMID:[Effect of lactitol (NS-4) on the increase in blood and brain ammonia concentration and on coma in newly developed rat models of hepatic coma]. 773 97

Animal models of chronic liver disease with hyperammonemia are currently available to investigators. Two in particular have been utilized extensively. Carbon tetrachloride induced (CCl4) cirrhosis in the rat and portacaval shunt in the same species and other animals particularly the dog. In regards to hepatic encephalopathy, however, the CCl4 cirrhosis rat model seems to display few behavioral changes unless very advanced decompensated cirrhosis is produced. Further work should be done on this model to verify the development of encephalopathy and to improve reproducibility. The portacaval shunt rat on the other hand clearly has a consistent albeit subtle set of behavioral changes. Recent improvements in detecting these changes and more importantly showing reversal or improvement by neomycin or a low protein diet are a major advance. Hopefully, more laboratories will be able to reproduce this reversible change in behavior. Experiences gained from 7 years of using the portacaval shunt rat and other models of liver disease are described.
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PMID:Animal models of hepatic encephalopathy and hyperammonemia. 774 Sep 98

The liver is a major parenchymal organ involved in many functional activities in the body. Hepatic encephalopathy is a syndrome characterized by increased blood ammonia level and is one of the major complications of cirrhosis. In the present study the protective effect of HD-03, a poly-herbal formulation, was evaluated against CCl4-induced hepatic encephalopathy in rats. Hepatic encephalopathy was induced in Wistar rats by administration of CCl4 at a dose of 1 mL/kg orally in liquid paraffin (1:1) twice a week for 90 days. The liver enzymes (SGPT and SGOT) and blood ammonia levels were significantly (p < 0.001) higher in the CCl4-intoxicated group compared with the untreated control group. Administration of HD-03 at a dose of 750 mg/kg orally as an aqueous suspension significantly prevented the elevation of SGPT, SGOT and blood ammonia levels. Histomorphometric evaluation of liver and brain showed a protective effect of the HD-03 treatment, thus correlating with the changes in biochemical profiles. The protective effect of HD-03 against CCl4-induced encephalopathy may be due to the improved hepatocellular function, which in turn helps in regulating the metabolism of ammonia. However, further studies are required to measure the activity of enzymes involved in the urea cycle and brain aromatic amino acids in order to elucidate the exact mechanism of action of HD-03.
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PMID:The protective effect of HD-03 in CCl4-induced hepatic encephalopathy in rats. 1153 77

The review presents the modern concepts on biochemical mechanisms of processes, that result in comatose states (CS), with emphasis on the search of new therapeutic approaches. CS of various origin causes severe suppression of brain cells functioning and stable unconsciousness. Numerous reasons of various CS are classified into two main groups: primary brain damages (ischemia, tumor, trauma) and secondary damages originating from system injuries in the body (endocrine, toxic e. c.). The most often primary CS is the hypoxic-ischemic one, as result of corresponding encephalopathy. Its mechanism is the brain cells "energy crisis"--because of decreased blood supply or its deficiency by energy substrates or/and by oxygen. Among secondary CS the substantial place takes hepatic coma as a consequence of hepatic encephalopathy in severe liver diseases--cirrhosis, acute liver failure, sharp intoxication. Its main reason is associated with exess of ammonia entering the brain tissue (it accumulates in blood because of lack of its removing by damaged hepatocytes). Ammonia reacts with glutamate in brain astrocytes and the product of this reaction, glutamine, induced osmotic imbalance, that results in change of form and functions of these important brain cells. It induces, in turn, neurons functions damages, changes in neurotransmission and cerebral blood flow and all these may give rise CS. The most of CS studies are carried out in human. Experimental models ofhepatic CS are reproduced mainly in rats, the most often by surgery methods. Other models included administration of thioacetamide or D-galactosamine, sometimes in combination with lipopolysaccharide. In earlier studies ammonia administration together with liver damages by ligation or by CCl4 was used. The main principles of hepatic coma treatment include the care of encephalopathy, detoxification, and liver treatment. Elaboration of new nanodrugs with increased penetration into tissues and cells, in particular, on the base of phospholipid nanoparticles, may increase substantially the therapeuti efficiency. One of such drug is thought to be a new hepatoprotective preparation phosphogliv--nanoparticles of soy phosphatidylcholine with glycyrrhizic acid. It is supposed, that the further development of phospholipid nanoforms, with minimal particle sizes, may reveal the more action in CS treatment.
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PMID:[Comatose states: etiopathogenesis, experimental studies, treatment of hepatic coma]. 2000 Jan 19