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Hepatic encephalopathy: Ever closer to its big bang

World Journal of Gastroenterology 2016年第42期22卷 9251-9256页

作者： Pablo A Souto Ariel R Marcotegui Lisandro Orbea juan Skerl juan carlos perazzo Department of Pathology Laboratory of Hyperammonemia and Hepatic Encephalopathy Center of Applied and Experimental Pathology Faculty of Medicine University of Buenos Aires

Hepatic encephalopathy(HE) is a neuropsychiatric disorder that commonly complicates the course of patients with liver disease. Despite the fact that the syndrome was probably first recognized hundreds of years ago, the exact pathogenesis still remains unclear. Minimal hepatic encephalopathy(MHE) is the earliest form of HE and is estimated to affect more that 75% of patients with liver cirrhosis. It is characterized by cognitive impairment predominantly attention, reactiveness and integrative function with very subtle clinical manifestations. The development of MHE is associated with worsen in driving skills, daily activities and the increase of overall mortality. Skeletal muscle has the ability to shift from ammonia producer to ammonia detoxifying organ. Due to its large size, becomes the main ammonia detoxifying organ in case of chronic liver failure and muscular glutaminesynthase becomes important due to the failing liver and brain metabolic activity. Gut is the major glutamine consumer and ammonia producer organ in the body. Hepatocellular dysfunction due to liver disease, results in an impaired clearance of ammonium and in its interorgan trafficking. Intestinal bacteria, can also represent an extra source of ammonia production and in cirrhosis, small intestinal bacterial overgrowth and symbiosis can be observed. In the study of HE, to get close to MHE is to get closer to its big bang; and from here, to travel less transited roads such as skeletal muscle and intestine, is to go even closer. The aim of this editorial is to expose this road for further and deeper work.

关键词： Ammonia Skeletal muscle Minimal hepatic encephalopathy Hyperammonemia

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Hepatic encephalopathy:An approach to its multiple pathophysiological features

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World Journal of Hepatology 2012年第3期4卷 50-65页

作者： juan carlos perazzo Silvina Tallis Amalia Delfante Pablo Andrés Souto Abraham Lemberg Francisco Xavier Eizayaga Salvador Romay Laboratory of Portal Hypertensionand Hepatic Encephalopathy PathophysiologySchool of Pharmacy and BiochemistryUniversity of Buenos Aires Laboratory of Experimental Pathology School of MedicineUniversity of Buenos Aires Clinical Unit General Hospital I PirovanoGCBA

Hepatic encephalopathy(HE)is a neuropsychiatric complex syndrome,ranging from subtle behavioral abnormalities to deep coma and *** encephalopathy emerges as the major complication of acute or chronic liver *** of factors are involved in its pathophysiology,such as central and neuromuscular neurotransmission disorder,alterations in sleep patterns and cognition,changes in energy metabolism leading to cell injury,an oxidative/nitrosative state and a neuroinflammatory ***,in acute HE,a condition of imminent threat of death is present due to a deleterious astrocyte *** chronic HE,changes in calcium signaling,mitochondrial membrane potential and long term potential expression,N-methyl-D-aspartate-cGMP and peripheral benzodiazepine receptors alterations,and changes in the mRNA and protein expression and redistribution in the cerebral blood flow can be *** main molecule indicated as responsible for all these changes in HE is *** is no doubt that ammonia,a neurotoxic molecule,triggers or at least facilitates most of these *** plasma levels are increased two-to three-fold in patients with mild to moderate cirrhotic HE and up to ten-fold in patients with acute liver failure. Hepatic and inter-organ trafficking of ammonia and its metabolite,glutamine(GLN),lead to hyperammonemic *** of hepatic ammonia is a differentiated work that includes the hepatocyte,through the urea cycle,converting ammonia into GLN via glutamine *** pathological conditions,such as liver damage or liver blood bypass,the ammonia plasma level starts to rise and the risk of HE developing is high. Knowledge of the pathophysiology of HE is rapidly expanding and identification of focally localized triggers has led the development of new possibilities for HE to be *** editorial will focus on issues where, to the best of our knowledge,more research is needed in order to clarify,at least partially

关键词： Liver failure Hepatic encephalopathy Ammonia and central nervous system Hyperammonemia

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Antioxidant role of heme oxygenase-1 in prehepatic portal hypertensive rats

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World Journal of Gastroenterology 2006年第26期12卷 4149-4155页

作者： Soledad Gonzales María Julia Pérez juan C perazzo María Luján Tomaro Department of Biological Chemistry School of Pharmacy and Biochemistry University of Buenos AiresBuenos Aires 1113Argentina Laboratory of Portal Hypertension Department of Biological Science School of Pharmacy and BiochemistryUniversity of Buenos AiresBuenos Aires 1113Argentina

AIM： To study the effect of bilirubin on the oxidative liver status and the activity and expression of heine oxygenase-1 （HO-1） in rat liver injury induced by prehepatic portal hypertension. METHODS： Wistar male rats, weighing 200-250 g, were divided at random into two groups： one group with prehepatic portal hypertension （PH） induced by regulated prehepatic portal vein ligation （PPVL） and the other group corresponded to sham operated rats. Portal pressure, oxidative stress parameters, antioxidant enzymes, HO-1 activity and expression and hepatic sinusoidal vasodilatation were measured. RESULTS： In PPVL rats oxidative stress was evidenced by a marked increase in thiobarbituric acid reactive substances （TBARS） content and a decrease in reduced glutathione （GSH） levels. The activities of liver antioxidant enzymes, superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GSH-Px） were also diminished while activity and expression of HO-1 were enhanced. Administration of bilirubin （5μmol/kg body weight） 24 h before the end of the experiment entirely prevented all these effects. Pretreatment with Sn-protoporphyrin IX （Sn-PPIX）（100 μg/kg body weight, i.p.）, a potent inhibitor of HO, completely abolished the oxidative stress and provoked a slight decrease in liver GSH levels as well as an increase in lipid peroxidation. Besides, carbon monoxide, another heme catabolic product, induced a significant increase in sinusoidal hepatic areas in PPVL group. Pretreatment of PPVL rats with Sn-PPIX totally prevented this effect CONCLUSION： These results suggest a beneficial role of HO-1 overexpression in prehepatic portal hypertensive rats.

关键词： Heme oxygenase-1 Portal hypertensive rats Liver oxidative stress

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Altered blood-brain barrier permeability in rats with prehepatic portal hypertension turns to normal when portal pressure is lowered

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World Journal of Gastroenterology 2006年第9期12卷 1367-1372页

作者： Francisco Eizayaga Camila Scorticati juan P Prestifilippo Salvador Romay Maria A Fernandez José L Castro Abraham Lemberg juan C perazzo Laboratory of Portal Hypertension Department of Pathophysiology School of Pharmacy and BiochemistryUniversity of Buenos AiresBuenos AiresArgentina Catedra de Farmacología School of Pharmacy and Biochemistry University of Buenos Aires Buenos Aires Argentina Laboratory of Portal Hypertension Department of Pathophysiology School of Pharmacy and Biochemistry University of Buenos Aires Buenos AiresArgentina

AIM： To study the blood-brain barrier integrity in prehepatic portal hypertensive rats induced by partial portal vein ligation, at 14 and 40 dafer ligation when portal pressure is spontaneously normalized. METHODS： Adult male Wistar rats were divided into four groups： Group Ⅰ： Sham14d, sham operated; Group Ⅱ： PHil, portal vein stenosis, （both groups were used 14 days after surgery）; Group Ⅲ： Sham4od, Sham operated and Group Ⅳ： PH4od Portal vein stenosis （Groups Ⅱ and Ⅳ used 40 d afer surgery）. Plasma ammonia, plasma and cerebrospinal fluid protein and liver enzymes concentrations were determined. Trypan and Evans blue dyes, systemically injected, were investigated in hippocampus to study blood-brain barrier integrity. Portal pressure was periodically recorded. RESULTS： Forty days afer stricture, portal pressure was normalized, plasma ammonia was moderately high, and both dyes were absent in central nervous system parenchyma. All other parameters were reestablished. When portal pressure was normalized and ammonia level was lowered, but not normal, the altered integrity of blood-brain barrier becomes reestablished. CONCLUSION： The impairment of blood-brain barrier and subsequent normalization could be a mechanism involved in hepatic encephalopathy reversibility. Hemodynamic changes and ammonia could trigger blood-brain barrier alterations and its reestablishment.

关键词： Blood-brain barrier Rats Prehepatic portal hypertension

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Hyperammonemia,brain edema and blood-brain barrier alterations in prehepatic portal hypertensive rats and paracetamol intoxication

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World Journal of Gastroenterology 2004年第9期10卷 1321-1324页

作者： Camila Scorticati juan P.Prestifilippo Francisco X.Eizayaga Salvador Romay MaríaA Fernández AbrahamLemberg juan C.perazzo José L.Castro Cátedra de Fisiopatología Facultad de Farmaciay BioquímicaUniversidad de Buenos AiresBuenos AiresArgentina Cátedra de Farmacología Facultad de Farmacia y BioquímicaUniversidad de Buenos AiresBuenos AiresArgentina

AIM:To study the blood-brain barrier integrity,brain edema, animal behavior and ammonia plasma levels in prehepatic portal hypertensive rats with and without acute liver intoxication. METHODS:Adults male Wistar rats were divided into four *** Ⅰ:sham operation;Ⅱ:Prehepatic portal hypertension,produced by partial portal vein ligation;Ⅲ: Acetaminophen intoxication and Ⅳ:Prehepatic portal hypertension plus *** was administered to produce acute hepatic *** pressure,liver serum enzymes and ammonia plasma levels were *** cortex water content was registered and trypan blue was utilized to study blood brain barrier *** and behavioral tests were recorded. RESULTS:Portal hypertension was significantly elevated in groups Ⅱ and Ⅳ.Uver enzymes and ammonia plasma levels were increased in groups Ⅱ,Ⅲ and Ⅳ.Prehepatic portal hypertension (group Ⅱ),acetaminophen intoxication (group Ⅲ) and both (group Ⅳ) had changes in the blood brain-barrier integrity (trypan blue) and *** edema was present in rats with acute hepatic injury in groups Ⅲ and Ⅳ.Behavioral test (rota rod) was altered in group Ⅳ. CONCLUSION:These results suggest the possibility of another pathway for cortical edema production because blood brain barrier was altered (vasogenic) and hyperammonemia was registered (oltotoxic).Group Ⅳ,with behavioral altered test,can be considered as a model for study at an early stage of portal-systemic encephalopathy.

关键词： Acetaminophen Analgesics, Non-Narcotic Animals Behavior, Animal Blood-Brain Barrier Brain Edema Humans Hyperammonemia Hypertension, Portal Liver Male Rats Rats, Wistar

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