Exogenous Hydrogen Sulfide Protects Against Traumatic Hemorrhagic Shock Via Attenuation of Oxidative Stress

ObjectiveThis study was designed to investigate the protective effects of exogenous hydrogen sulfide (H2S) on trauma-hemorrhagic shock (T-H).Materials and MethodsForty-eight male Sprague-Dawley rats were anesthetized, while 32 were subjected to both midline laparotomy and hemorrhagic shock (35–40 mmHg for 90 min) by bleeding them from the femoral artery. One hour later, resuscitation was initiated with Ringer lactate. NaHS (28 μmol/kg) or vehicle alone was administered intraperitoneally at the onset of resuscitation. Two hours later, eight animals from each group were re-anesthetized to determine cardiac function, blood gas concentrations, and hepatic and renal function. Superoxide dismutase activity (SOD), malondialdehyde concentrations (MDA), and the activity of myeloperoxidase (MPO) in the serum were measured and pulmonary wet/dry (W/D) ratio and histopathologic evaluations performed.ResultsNaHS resulted in an increase in mean arterial blood pressure, left ventricular pressure and positive (+dP/dtmax) and negative (–dP/dtmax) first derivatives of pressure as compared with the vehicle only group. The pH, PaO2 and base excess (BE) were increased in the NaHS-treated group compared with the vehicle-treated group. Aspartate aminotransferase, alanine aminotransferase, blood urea nitrogen, and serum creatinine were reduced in the NaHS-treated group. NaHS also significantly reduced the high mortality rate at 24 h otherwise caused by T-H. The NaHS-treated group showed a remarkable decrease in MDA and MPO concentrations in plasma and an increase in SOD as compared with the vehicle-treated group. Histopathologic analysis indicated less edema, congestion, inflammatory cell infiltration and necrosis in heart, lung, liver and kidney tissue in NaHS-treated group.ConclusionsThe present study demonstrates that exogenous H2S administered at an appropriate dose confers protective effects after T-H and resuscitation, by preventing a decrease in the antioxidant defense system.