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AIM: To investigate the effect of sodium pentobarbitone (SP) or ketamine/xylazine (KX) anesthetics on acute gastric injury. METHODS: Portal hypertension was induced by bile duct ligation (BDL) or portal vein stenosis (PVS). Ethanol (EtOH)-induced gastric damage was assessed using ex vivo gastric chamber experiments. Gastric blood flow (GBF) was also measured by laser doppler flowmetry. RESULTS: EtOH-induced gastric damage was reduced in BDL rats under KX anesthesia in comparison to those under SP anesthesia. GBF dysfunction in fasted BDL rats was partially restored under KX anesthesia. In contrast, in fasted PVS rats, EtOH-induced gastric damage was increased under KX anesthesia while GBF was reduced. CONCLUSION: The use of KX anesthesia in experimental procedures involving cirrhotic rats (but not those with pure portal hypertension) is preferable to SP anesthesia.

AIM: To investigate the relationship between primary afferent neurons, endothelin (ET) and the role of its receptors on ethanol-induced gastric damage in cirrhotic rats. METHODS: Cirrhosis and portal hypertension were induced in rats by bile duct ligation (BDL) while controls had a sham operation. The association between ET and afferent neurons on the gastric mucosa was evaluated by capsaicin treatment in newborn rats, the use of ET agonists or antagonists, gastric ET-1 and -3 mRNA and synthetic capacity. Ethanol-induced damage was assessed using ex vivo gastric chamber experiments. Gastric blood flow was measured by laser-Doppler flowmetry. RESULTS: ET-3 and an ETB receptor antagonist significantly reduced the extent of ethanol-induced gastric damage in BDL rats. Gastric ET-1 and -3 levels were 30% higher in BDL rats compared to control rats. Capsaicin treatment restored the gastric resistance and blood flow responses to topical application of ethanol in BDL rats and ET-1 and -3 production to levels observed in controls. CONCLUSION: Our results suggest that the reduced resistance of the gastric mucosa of cirrhotic rats to ethanol-induced injury is a phenomenon modulated by ET through the ETB receptor and by sensory afferent neurons.