BACKGROUND: Amputation is a special type of trauma. Mechanism of trauma-induced damage to the liver and the effects of hydrogen sulfide (H2S) on the liver remain unclear.
OBJECTIVE: To explore the mechanism of hepatic damage in rats of postoperative amputation, and how H2S exerts effects on liver function.
METHODS: Wistar rats and Sprague-Dawley rats were equally and randomly divided into normal group, postoperative 6-, 12-, 24- and 72-hour groups, sodium hydrosulfide (NaHS) group, and propargyl glycine group, as well as normal group, postoperative 6-hour group, HaHS group, and propargyl glycine group. Except the normal group, the structure 1.2-1.4 cm above the left knee was completely transected in rats of other groups. Blood vessels were ligated, and then left femoral vein and femoral artery were cut to establish rat models of amputation in the left hind limb. In the NaHS and propargyl glycine groups, 28 µmol/kg NaHS and 50 mg/kg propargyl glycine were intraperitoneally injected immediately after amputation.
RESULTS AND CONCLUSION: Compared with the normal group, traumatic changes in rat liver cells and mitochondrial structure were seen, and plasma and liver myeloperoxidase, malondialdehyde, H2S/cystathionine γ-lyase levels, liver mitochondrial respiratory control rate, membrane potential and ATP activity were significantly lower in the postoperative 6-hour groups (P < 0.05). After NaHS intervention, H2S/cystathionine γ-lyase level and above indicators were significantly higher in the postoperative 6-hour groups (P < 0.05), but plasma transaminase did not significantly alter (P > 0.05). After treatment with propargyl glycine, above indicators except mitochondrial indexes were further decreased, and transaminase was significantly reduced (P < 0.05). These findings suggest
that H2S can reduce lipid peroxidation, inflammatory reaction, and make the mitochondrial function improved significantly, but did not reduce the damage of liver function in rat models after amputation.