Liver ischemia-reperfusion injury occurs in major liver resections and transplantation. Experimental studies verified a multistep process that ends in inflammation and hepatocellular necrosis.
AIM: To evaluate if the treatment of liver ischemia-reperfusion injury with sodium chloride hypertonic solution (HTS) prevents local and systemic damage.
Methods: Twenty-four Wistar male rats underwent partial liver ischemia performed by clamping the pedicle from medium and left anterior lateral segments during an hour under mechanical ventilation. They were divided in to 3 groups: group C (n=8): control rats submitted to partial liver ischemia; group HTS (n=8): rats received HTS (NaCl 7.5%) 0.4mL/Kg, 10 minutes before reperfusion; and group S (n=8): rats received normal saline solution (NaCl 0.9%) 3.4mL/Kg, 10 minutes before reperfusion. After four hours of reperfusion Evans blue was intravenously administrated and blood was collected. Rats were killed for liver histology, phosphorylation of liver mitochondria and pulmonary vascular permeability analyzes. Six rats were added to each group to determinate AST and ALT.
Results: Elevation of AST was similar in groups C and S (3141±1133U/L versus 3163±776U/L, p>0.05) and significantly higher than group HTS (1894±1775U/L, p<0.05). The same occurred with elevation of ALT (C: 2903±1299U/l versus S: 2728±873U/L versus HTS: 1539±777U/L, p<0.05). A significant reduction on mitocondrial dysfunction was observed in animals of group HTS compared with groups C and S (p<0.05). Pulmonary permeability was significantly higher in groups C and S compared with group HTS (p<0.05). No difference in liver necrosis was showed among groups C, HTS and S.
Conclusion: Administration of hypertonic saline solution in experimental rat model attenuated liver ischemia-reperfusion injury, ameliorating mitocondrial dysfunction and decreasing pulmonary vascular permeability. Supported by FAPESP n0 05/04226-7