OBJECTIVE: To investigate the effects of aminoguanidine on the lung injury induced by the total hepatic ischemia-reperfusion in rats. METHODS: The total hepatic ischemia-reperfusion model was built after blocking of the hepatic porta, suprahepatic and infrahepatic vena cava. Ninety Sprague-Dawley rats were assigned randomly into 3 groups: Sham operation group (Group A, n=30); total hepatic ischemia group (Group B, n=30); and aminoguanidine treatment group (Group C, n=30). Each group was subdivided randomly into 3 subgroups (n=10) according to different time phases: 20 minutes after the total hepatic vascular exclusion (T0), 4 hours after the reperfusion (T1), and 48 hours after the survival Group A and Group B were intravenously injected with normal saline ( mL/kg) while Group C was injected with aminoguanidine (20 mg/kg) dissolved in normal saline (1 mL/kg) 10 minutes before the open of the abdomin. The levels of portal blood nitric oxide ( O) endotoxin ( ET), tumor necrosis factor-alpha (TNF-alpha at T0 and T1 were detected; 48 hours survival rates and the lung wet/dry weight ratio were counted; and the histological changes of the lung tissues were observed. RESULTS: Compared with Group A, the levels of portal vein NO, ET, and TNF-alpha T0 and T1 in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). But those indexes of Group C were lower than those of Group B (P < 0.05). The 48-hour survival rate in Group C was higher than that in Group B (P < 0.05). The lung wet/dry weight ratio in Group C was lower than in Group B (P < 0.05) and the histological change of Group C was slighter than that in Group B. CONCLUSION: Aminoguanidine has the protective effects on the lungs against the total hepatic ischemia-reperfusion induced injury.
OBJECTIVE: To investigate the effects of aminoguanidine on the lung injury induced by the total hepatic ischemia-reperfusion in rats. METHODS: The total hepatic ischemia-reperfusion model was built after blocking of the hepatic porta, suprahepatic and infrahepatic vena cava. Ninety Sprague-Dawley rats were assigned randomly into 3 groups: Sham operation group (Group A, n=30); total hepatic ischemia group (Group B, n=30); and aminoguanidine treatment group (Group C, n=30). Each group was subdivided randomly into 3 subgroups (n=10) according to different time phases: 20 minutes after the total hepatic vascular exclusion (T0), 4 hours after the reperfusion (T1), and 48 hours after the survival Group A and Group B were intravenously injected with normal saline ( mL/kg) while Group C was injected with aminoguanidine (20 mg/kg) dissolved in normal saline (1 mL/kg) 10 minutes before the open of the abdomin. The levels of portal blood nitric oxide ( O) endotoxin ( ET), tumor necrosis factor-alpha (TNF-alpha at T0 and T1 were detected; 48 hours survival rates and the lung wet/dry weight ratio were counted; and the histological changes of the lung tissues were observed. RESULTS: Compared with Group A, the levels of portal vein NO, ET, and TNF-alpha T0 and T1 in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). But those indexes of Group C were lower than those of Group B (P < 0.05). The 48-hour survival rate in Group C was higher than that in Group B (P < 0.05). The lung wet/dry weight ratio in Group C was lower than in Group B (P < 0.05) and the histological change of Group C was slighter than that in Group B. CONCLUSION:Aminoguanidine has the protective effects on the lungs against the total hepatic ischemia-reperfusion induced injury.