论文部分内容阅读
AIM:To study the blood-brain barrier integrity,brain edema,animal behavior and ammonia plasma levels in prehepatic portalhypertensive rats with and without acute liver intoxication.METHODS:Adults male Wistar rats were divided into fourgroups.Group Ⅰ:sham operation;Ⅱ:Prehepatic portalhypertension,produced by partial portal vein ligation;Ⅲ:Acetaminophen intoxication and Ⅳ:Prehepatic portalhypertension plus acetaminophen.Acetaminophen wasadministered to produce acute hepatic injury.Portalpressure,liver serum enzymes and ammonia plasma levelswere determined.Brain cortex water content was registeredand trypan blue was utilized to study blood brain barrierintegrity.Reflexes and behavioral tests were recorded.RESULTS:Portal hypertension was significantly elevated ingroups Ⅱ and Ⅳ.Uver enzymes and ammonia plasma levelswere increased in groups Ⅱ,Ⅲ and Ⅳ.Prehepatic portalhypertension (group Ⅱ),acetaminophen intoxication (groupⅢ) and both (group Ⅳ) had changes in the blood brain-barrierintegrity (trypan blue) and hyperammonemia.Cortical edemawas present in rats with acute hepatic injury in groups Ⅲ andⅣ.Behavioral test (rota rod) was altered in group Ⅳ.CONCLUSION:These results suggest the possibility ofanother pathway for cortical edema production because bloodbrain barrier was altered (vasogenic) and hyperammonemiawas registered (oltotoxic).Group Ⅳ,with behavioral alteredtest,can be considered as a model for study at an earlystage of portal-systemic encephalopathy.
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 groups. Group I: sham operation; II: Prehepatic portal hypertensive, produced by partial portal vein ligation; III: Acetaminophen intoxication and IV: Prehepatic portal hypertypeension plus acetaminophen. Acetaminophen was administered to produce acute hepatic injury. Portal pressure, liver serum enzymes and ammonia plasma levels were determined. Brain cortex water content was registered and trypan blue was utilized to study blood brain barrier integrity. Reflexes 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. Parenteral hyperthension (group II), acetaminophen intoxication (group Ⅲ) and both (group Ⅳ) had changes in the blood brain-barrier integrity (trypan blue) and hyperammonemia. Cortical 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 path for cortical edema production because Group B, with behavioral altered test, can be considered as a model for study at an early stage of portal-systemic encephalopathy.