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Modifications produced by selective inhibitors of cyclooxygenase and ultra low dose aspirin on platelet activity in portal hypertension

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World Journal of Gastroenterology 2007年第38期13卷 5065-5070页

作者： francisco x eizayaga Omar Aguejouf Vanessa Desplat Philippe Belon Christian Doutremepuich CEBBAD Universidad Maimónides Buenos Aires Argentina France Laboratoire d'Hématologie Université Victor Segalen Bordeaux 2 Bordeaux 146 Rue Léo Saignat 33076 Bordeaux Cedex France Laboratoires Boiron Sainte-Foy-les-Lyons France

AIM: To study the mechanism involved in the potentially beneficial effect of ultra low dose aspirin (ULDA) in prehepatic portal hypertension, rats were pretreated with selective COx 1 or 2 inhibitors (SC-560 or NS-398 respectively), and subsequently injected with ULDA or placebo. METHODS: Portal hypertension was induced by portal vein ligation. Platelet activity was investigated with an in-vivo model of laser induced thrombus production in mesenteric circulation and induced hemorrhagic time (IHT). Platelet aggregation induced by ADP and dosing of prostanoid products 6-keto-PGF1α, TxB2, PGE2 and LTB4 were also performed. RESULTS: The portal hypertensive group receiving a placebo showed a decreased in vivo platelet activity with prolonged IHT, an effect that was normalized by ULDA. SC-560 induced a mild antithrombotic effect in the normal rats, and an unmodified effect of ULDA. NS-398 had a mild prothrombotic action in portal hypertensive rats, similar to ULDA, but inhibited a further effect when ULDA was added. An increased 6-keto-PGF1α was observed in portal hypertensive group that was normalised after ULDA administration. TxA2 level after ULDA, remained unchanged. CONCLUSION: These results suggest that the effect of ULDA on platelet activity in portal hypertensive rats, could act through a COx 2 pathway more than the COx 1, predominant for aspirin at higher doses.

关键词： Ultra Low Dose Aspirin Portal hypertension COx 1 COx 2 COx selective inhibition

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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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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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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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