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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several reports have demonstrated the alleviation of hepatic encephalopathy by flumazenil, an antagonist of benzodiazepine receptors. As changes in central monoaminergic activity are involved in the mechanisms for hepatic encephalopathy, the effects of flumazenil on central monoaminergic activity were evaluated in acute hepatic failure produced by ischemia-reperfusion injury in rats. Eighteen male Wistar rats were evenly assigned to three groups: sham-operated group given saline, liver-ischemic group given saline, and liver-ischemic group given flumazenil. Flumazenil (1 mg/kg) or saline (10 mL/kg) was intraperitoneally administered three times, at 1, 6, and 24 hours after 90 minutes of liver ischemia produced by occlusion of the left portal vein. The extracellular concentrations of neurotransmitter amino acids, monoamines, and their metabolites were determined in the striatum using a microdialysis procedure. Another set of 12 rats was subjected to liver ischemia, and the effect of flumazenil on spontaneous motor activity was examined after 24 hours. The extracellular concentration of 3,4-dihydroxyphenylacetic acid, a metabolite of dopamine, decreased to 39% of that in sham-operated animals 24 hours after surgery (P < 0.05), although the dopamine level did not change. The treatment with flumazenil completely abolished the decrease in the metabolite (P < 0.05). Although the glutamate level in the injured animals decreased to 42% of that in sham-operated animals (P < 0.05), no remarkable increase in the glutamate level was observed in animals treated with flumazenil. Spontaneous motor activity decreased 24 hours after surgery in animals subjected to liver ischemia. Flumazenil led to improvement of spontaneous motor activity 5 minutes after administration, but this effect was not observed after 30 minutes. The restoration of the central dopaminergic function may be a contributing factor in the improvement of hepatic encephalopathy.
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PMID:Flumazenil-induced improvement of the central dopaminergic system in rats with acute hepatic failure. 1584 Sep 91

A hypothesis about the inflammatory etiopathogeny mediated by astroglia of hepatic encephalopathy is being proposed. Three evolutive phases are considered in chronic hepatic encephalopathy: an immediate or nervous phase with ischemia-reperfusion, which is associated with reperfusion injury, edema and oxidative stress; an intermediate or immune phase with microglia hyperactivity, which produces cytotoxic cytokines and chemokines and is involved in enzyme hyperproduction and phagocytosis; and a late or endocrine phase, in which neuroglial remodeling, with an alteration of angiogenesis and neurogenesis, stands out. The increasingly complex trophic meaning that the metabolic alterations have in the successive phases making up this chronic inflammation could explain the metabolic regression produced in acute and acute-on-chronic hepatic encephalopathy. In these two types of hepatic encephalopathy, characterized by edema, neuronal nutrition by diffusion would guarantee an appropriate support of substrates, in accordance with the reduced metabolic needs of the cerebral tissue.
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PMID:The inflammatory bases of hepatic encephalopathy. 1709 80

A decrease in the serum ratio of branched-chain amino acids (BCAAs) to aromatic amino acids (Fischer ratio) reflects the severity of hepatic encephalopathy, and clinical improvement by dietary augmentation with BCAAs has been demonstrated. As behavioral alteration results from changes in central neurotransmission, we investigated the role of BCAA administration on changes in the levels of central neurotransmitters in acute liver injury. Male Wistar rats were subjected to liver ischemia by occluding the left portal vein and hepatic artery for 90 minutes. A 4% BCAA solution containing valine, leucine, and isoleucine was intraperitoneally administered 3 times (8 mL/kg, each) at 1 hour, 6 hours, and 24 hours after vascular reperfusion, and changes in the extracellular concentrations of neurotransmitter amino acids, monoamines, and their metabolites were evaluated in the striatum by a microdialysis procedure. Although the extracellular concentration of dopamine was affected by neither liver ischemia nor BCAA injections, the level of 3,4-dihydroxyphenylacetic acid, a metabolite of dopamine, decreased to 34% in the ischemic group 24 hours after reperfusion. The 3,4-dihydroxyphenylacetic acid level was normalized by treatments with BCAAs. The improvement of deranged cerebral dopaminergic activity may be a contributing factor in the improvement of hepatic encephalopathy by BCAAs.
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PMID:Recovery of brain dopamine metabolism by branched-chain amino acids in rats with acute hepatic failure. 1789 76

Despite recent advances in the understanding of mechanisms underlying the pathogenesis of liver diseases, therapeutic agents are still needed in several instances such as nonalcoholic fatty liver disease, alcoholic liver disease or fibrogenesis associated with chronic liver injury. Over the past decades, cannabinoid receptors have emerged as critical mediators of acute and chronic liver injury, and pharmacological modulation of these receptors has demonstrated efficacy in preclinical models of nonalcoholic and alcoholic fatty liver, fibrosis, liver ischemia reperfusion and of complications of cirrhosis, including cirrhotic portal hypertension, cirrhotic cardiomyopathy and hepatic encephalopathy. Moreover, CB(1) antagonists have entered clinical trials for the management of nonalcoholic steatohepatitis. This review will depict the pleiotropic functions of cannabinoid receptors in liver disease and highlight potential therapeutic applications, some of which may be available in the near future.
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PMID:Cannabinoid receptors as therapeutic targets in the management of liver diseases. 1925 49

A 60-year-old woman with hepatic encephalopathy was admitted to our hospital. Ultrasonography, computed tomography and hepatic arteriography revealed diffuse hepatic arteriovenous fistulae (HAVF). Overt portosystemic shunt could not be identified. Right heart catheterization showed increased cardiac output. However the patient had never shown any signs of heart failure. Other than that, marked hepatopetal arterial flow from some branches of the superior mesenteric artery was detected and mesenteric arterial flow remarkably decreased. Extensive HAVF can lead to significant complications, including high output heart failure, pulmonary hypertension, portal hypertension, hepatic encephalopathy, biliary ischemia, cirrhosis, postprandial abdominal pain, and reduced liver function. Embolization or ligation of the hepatic artery provides temporal improvement of clinical symptoms, but long-term results are unsatisfactory because of the development of collateral circulation and the risk of refractory intrahepatic cholangitis, subsequently leading to liver failure. Liver transplantation offers another therapeutic option and can be a successful curative treatment.
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PMID:[A case of diffuse hepatic arteriovenous fistulae with hepatic encephalopathy, postprandial abdominal pain and biliary injury]. 1957 12

Hypothermia is a well established cytoprotectant, with remarkable and consistent effects demonstrated across multiple laboratories. At the clinical level, it has recently been shown to improve neurological outcome following cardiac arrest and neonatal hypoxia-ischemia. It is increasingly being embraced by the medical community, and could be considered an effective neuroprotectant. Conditions such as brain injury, hepatic encephalopathy and cardiopulmonary bypass seem to benefit from this intervention. It's role in direct myocardial protection is also being explored. A review of the literature has demonstrated that in order to appreciate the maximum benefits of hypothermia, cooling needs to begin soon after the insult, and maintained for relatively long period periods of time. In the case of ischemic stroke, cooling should ideally be applied in conjunction with the re-establishment of cerebral perfusion. Translating this to the clinical arena can be challenging, given the technical challenges of rapidly and stably cooling patients. This review will discuss the application of hypothermia especially as it pertains to its effects neurological outcome, cooling methods, and important parameters in optimizing hypothermic protection.
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PMID:Hypothermia as a cytoprotective strategy in ischemic tissue injury. 1983 33

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

Parenteral nutrition (PN) is indicated in alcoholic steatohepatitis (ASH) and in cirrhotic patients with moderate or severe malnutrition. PN should be started immediately when sufficientl oral or enteral feeding is not possible. ASH and cirrhosis patients who can be sufficiently fed either orally or enterally, but who have to abstain from food over a period of more than 12 hours (including nocturnal fasting) should receive basal glucose infusion (2-3 g/kg/d). Total PN is required if such fasting periods last longer than 72 h. PN in patients with higher-grade hepatic encephalopathy (HE); particularly in HE IV degrees with malfunction of swallowing and cough reflexes, and unprotected airways. Cirrhotic patients or patients after liver transplantation should receive early postoperative PN after surgery if they cannot be sufficiently rally or enterally nourished. No recommendation can be made on donor or organ conditioning by parenteral administration of glutamine and arginine, aiming at minimising ischemia/reperfusion damage. In acute liver failure artificial nutrition should be considered irrespective of the nutritional state and should be commenced when oral nutrition cannot be restarted within 5 to 7 days. Whenever feasible, enteral nutrition should be administered via a nasoduodenal feeding tube.
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PMID:Hepatology - Guidelines on Parenteral Nutrition, Chapter 16. 2004 84

A 64-year-old female with a history of primary biliary cirrhosis and esophageal varices starting at age 39 was brought to our Stroke Care Unit by ambulance with right-side weakness and speech difficulty. Physical examination revealed right hemiparesis (including the face), sensory disturbances, pathological reflexes, and slightly decreased consciousness, with a Glasgow Coma Scale rating of E3V4M6. Flapping tremors and speech disturbance, as well as anarithmia, construction apraxia, and ideomotor apraxia, were noted, and her National Institutes of Health Stroke Scale score was 13. Initially, the patient was diagnosed with acute stroke and treated accordingly; however, subsequent findings from clinical images and electroencephalography led to a diagnosis of focal neurologic signs due to hepatic encephalopathy (HE). The patient had significantly reduced cerebral blood flow in the left side of the brain, probably due to microsurgical repair of an aneurysm done 2 years earlier. HE with exaggerated chronic liver damage might have made the previously silent ischemia clinically apparent. This interpretation is supported by the fact that the patient's neurologic deficits resolved once HE was adequately controlled. This case illustrates the need for careful assessment of background pathophysiology when diagnosing patients with stroke-like symptoms.
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PMID:Hepatic encephalopathy with reversible focal neurologic signs resembling acute stroke: case report. 2063 97

Astrocytes assume multiple roles in maintaining an optimally suited milieu for neuronal function. Select astrocytic functions include the maintenance of redox potential, the production of trophic factors, the regulation of neurotransmitter and ion concentrations, and the removal of toxins and debris from the cerebrospinal fluid (CSF). Impairments in these and other functions, as well as physiological reactions of astrocytes to injury, can trigger or exacerbate neuronal dysfunction. This review addresses select metabolic interactions between neurons and astrocytes and emphasizes the role of astrocytes in mediating and amplifying the progression of several neurodegenerative disorders, such as Parkinson's disease (PD), hepatic encephalopathy (HE), hyperammonemia (HA), Alzheimer's disease (AD), and ischemia.
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PMID:Role of astrocytes in brain function and disease. 2107 20


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