BACKGROUND:Amputation is a special type of trauma. Mechanism of trauma-induced damage to the liver and the effects of hydrogen sulfide (H 2 S) on the liver remain unclear.
OBJECTIVE:To explore the mechanism of hepatic damage in rats of postoperative amputation, and how H 2 S exerts effects on liver function.
METHODS:Wistar rats and Sprague-Dawley rats were equal y and randomly divided into normal group, postoperative 6-, 12-, 24-and 72-hour groups, sodium hydrosulfide (NaHS) group, and propargyl glycine group, as wel 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 intraperitoneal y injected immediately after amputation.
RESULTS AND CONCLUSION:Compared with the normal group, traumatic changes in rat liver cel s and mitochondrial structure were seen, and plasma and liver myeloperoxidase, malondialdehyde, H 2 S/cystathionineγ-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, H 2 S/cystathionineγ-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 H 2 S 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.

Objective To investigate the protective mechanism of hydrogen sulfide(H2S) on inflammatory and oxidative damage of myocardium due to stress after amputation,and explore the relationship between H2S signal pathway and inflammatory and oxidative damage.Methods Twenty-eight adult male Wistar rats(weighing 260-300g) were randomly divided into 4 groups(7 each):control group,trauma group,NaHS group and PPG group.Rat model of traumatic stress was established in the rats in the 3 latter groups,and the animals were sacrificed 6 hours after modeling.The rats in control group were also sacrificed at the same time point.Rats in NaHS and PPG group respectively received intraperitoneal injection of NaHS(28?mol/kg) or PPG(50mg/kg).The level of H2S in plasma was measured by sensitive sulphur electrode,the activity of CSE in myocardium was determined by methylene blue method,myeloperoxidase(MPO) in plasma and myocardium was measured with ultraviolet spectrophotometry,and malondialdehyde(MDA) in plasma and myocardium was measured by TBA method.Results Compared with the control group,the content of H2S in plasma decreased,MPO and MDA in plasma and myocardium increased 6 hours after amputation(trauma group).Compared with the trauma group,the contents of H2S and MPO in plasma and the activity of CSE in myocardium increased,MDA in plasma and MPO and MDA in myocardium decreased in NaHS group,while the contents of H2S and MPO in plasma and the activity of CSE in myocardium decreased,MDA in plasma and MPO and MDA in myocardium increased in PPG group.Conclusion Inflammatory and oxidation injuries may occur in rat's myocardium after amputation,and H2S can offer a protective effect on myocardium by decreasing inflammatory and oxidative damage.

OBJECTIVETo explore the mechanism of kidney injury in rats following amputation and the protective effects of sodium hydrosulfide (NaHS) on kidney structure and function.

METHODSMale Wistar rats were randomly divided into normal control, 6 h after operation, NaHS intervention, and propargyl glycine (PPG) intervention groups (n=7). Plasma level of H2S, kidney injury molecule-1 (KIM-1), myeloperoxidase enzyme (MPO), malondialdehyde (MDA), nitric oxide (NO), urea nitrogen, creatinine, and renal tissue MPO, MDA, and KIM-1 levels, and activity of CSE were measured and the renal histological and mitochondrial structural changes were observed using optical and electron microscopy. In another experiment with SD rats, the rats were randomized also into these 4 groups (n=8) for measurement of renal mitochondrial respiratory control ratio, membrane potential and ATP activity.

RESULTSTraumatic changes in rat kidney cells and mitochondrial structure occurred in the rats 6 h after amputation with significantly increased plasma and renal KIM-1 (P<0.01) but significantly decreased H2S/CSE levels (P<0.01). Plasma H2S/kidney CSE level was significantly increased following NaHS intervention (P<0.01), which reduce the damage of the kidney tissue and significantly lower plasma and renal KIM-1, NO, BUN, Cr, MPO, and MDA (P<0.01). Rat kidney mitochondrial respiratory control ratio, membrane potential and ATP activity all decreased significantly after amputation (P<0.01) increased significantly after the application of NaHS; such improvements did not occur following PPG treatment.

CONCLUSIONSAmputation can lead to damage to the structure and function of the rat kidneys, and NaHS can significantly improve mitochondrial function and further reduce renal structural and functional impairments, suggesting that H2S, as an endogenous mediator, may act on the mitochondria through several pathways to regulate energy metabolism and participate in the pathophysiological processes of tissue damage and repair.

Acute Kidney Injury ; metabolism ; pathology ; prevention & control ; Amputation ; adverse effects ; Animals ; Creatinine ; blood ; Kidney ; metabolism ; pathology ; Male ; Malondialdehyde ; blood ; Nitric Oxide ; blood ; Peroxidase ; blood ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Sulfides ; therapeutic use