AIM: To study the effects of N-acetylcysteine and ischemic preconditioning on the portal triad clamping compared to arterial and portal clamping alone. METHODS: Eighty EPM 1-Wistar rats were randomized into two groups, depending on inclusion (Group 1) or not (Group 2) of the bile duct in the hepatic vascular pedicle occlusion. Each group was divided into four subgroups as follows. IR 1: 20 minutes after celiotomy, the pedicle containing vascular elements and bile duct to the left lateral and median liver lobes was occluded for 40 minutes, followed by 30 minutes of reperfusion. IPC 1: after 10 minutes of ischemia and 10 minutes of reperfusion, the ischemic preconditioning period, the rats were submitted to the same procedure described for IR 1 Group. NAC 1: the rats received N-acetylcysteine (150 mg/kg) 15 minutes before 40 minutes of ischemia and 5 minutes before 30 minutes of reperfusion. SHAM 1: The hepatic pedicle for the lateral and median liver lobes was dissected after 20 minutes, the bile duct alone was clamped for 40 minutes, and released for an additional 30 minutes. In the IR 2, IPC 2, and NAC 2 groups, ischemia was achieved with an exclusive vascular occlusion. SHAM 2: dissection and observation for 90 minutes. The blood was sampled for liver enzyme levels. Statistical analysis was done (P </= .05). RESULTS: Hepatic IR injury was less severe for animals from the classic portal triad clamping (group 1), with regard to AST (IR 1 Group 766 vs IR 2 Group 1380 U/L) and ALT (IR 1 Group 840 vs IR 2 Group 1576 U/L); IPC, but not NAC administration, was able to protect the liver from IR injury for animals from the classic portal triad clamping group, with regard to AST (IPC 1 Group 421 vs NAC 1 Group 1131 U/L) and ALT (IPC 1 Group 315 vs NAC 1 Group 1085 U/L). CONCLUSIONS: IPC protects the liver from IR injury; classic portal triad clamping results in a less severe hepatic IR injury when compared to bile duct exclusion.
AIM: To study the effects of N-acetylcysteine and ischemic preconditioning on the portal triad clamping compared to arterial and portal clamping alone. METHODS: Eighty EPM 1-Wistar rats were randomized into two groups, depending on inclusion (Group 1) or not (Group 2) of the bile duct in the hepatic vascular pedicle occlusion. Each group was divided into four subgroups as follows. IR 1: 20 minutes after celiotomy, the pedicle containing vascular elements and bile duct to the left lateral and median liver lobes was occluded for 40 minutes, followed by 30 minutes of reperfusion. IPC 1: after 10 minutes of ischemia and 10 minutes of reperfusion, the ischemic preconditioning period, the rats were submitted to the same procedure described for IR 1 Group. NAC 1: the rats received N-acetylcysteine (150 mg/kg) 15 minutes before 40 minutes of ischemia and 5 minutes before 30 minutes of reperfusion. SHAM 1: The hepatic pedicle for the lateral and median liver lobes was dissected after 20 minutes, the bile duct alone was clamped for 40 minutes, and released for an additional 30 minutes. In the IR 2, IPC 2, and NAC 2 groups, ischemia was achieved with an exclusive vascular occlusion. SHAM 2: dissection and observation for 90 minutes. The blood was sampled for liver enzyme levels. Statistical analysis was done (P </= .05). RESULTS: Hepatic IR injury was less severe for animals from the classic portal triad clamping (group 1), with regard to AST (IR 1 Group 766 vs IR 2 Group 1380 U/L) and ALT (IR 1 Group 840 vs IR 2 Group 1576 U/L); IPC, but not NAC administration, was able to protect the liver from IR injury for animals from the classic portal triad clamping group, with regard to AST (IPC 1 Group 421 vs NAC 1 Group 1131 U/L) and ALT (IPC 1 Group 315 vs NAC 1 Group 1085 U/L). CONCLUSIONS: IPC protects the liver from IR injury; classic portal triad clamping results in a less severe hepatic IR injury when compared to bile duct exclusion.
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