Table 1.

Protective effects of hydrogen sulfide during organ storage and transplantation

Organ	Experimental conditions	Findings	Reference
Heart	Isolated rat hearts; Langendorff perfusion system; Krebs–Henseleit solution. Cold heart storage for 6 h, followed by warm reperfusion for 30 min with or without sulfide (1 μM).	Sulfide accelerated the recovery of contractility during reperfusion, improved myocardial contractility, increased ATP content and decreased myocardial apoptosis index.	Hu et al., 2007.
Lung	Rabbit heart/lung blocs stored in cold low-potassium dextrane sulfate solution for 18 h, followed by a 2 h reperfusion with donor blood in an in vitro perfusion system. Lungs from donor animals ventilated with room were compared with lungs of donor animals ventilated for 1 h with 150 p.p.m. H2S prior to the start of the excision/storage of the heart/lung blocs.	Perfusion pressures were improved in the sulfide group. In addition, H2S-treated lungs had better oxygenation and ventilation indices. Finally, sulfide treatment reduced ROS formation during reperfusion and resulted in a better maintenance of mitochondrial cytochrome c content.	George et al., 2012.
	Rabbit heart/lung blocs stored in cold Perfadex solution for 18 h, followed by a 2 h reperfusion with donor blood in an in vitro perfusion system in the presence or absence of a bolus dose of NaHS (100 μg·kg−1 bolus + 1 mg·kg−1·h−1 infusion) starting at reperfusion.	Sulfide treatment reduced reactive oxygen species formation during reperfusion. Perfusion pressures were similar in all groups.	George et al., 2012.
	Single left lung transplantation in rats, with 3 h of cold storage/ischaemia. NaHS was administered to the recipient animal at 14 μmol·kg−1 15 min before the start of the transplantation.	Sulfide improved pulmonary function (e.g. PaO2/FiO2 ratio) and pulmonary histology, reduced lung oedema formation and reduced the accumulation of neutrophils in the lung. Sulfide resulted in a reduction in IL-1β and an increase in IL-10 levels.	Wu et al., 2013.
Kidney	Porcine kidneys subjected to 25 min of warm ischaemia followed by 18 h of cold storage on ice after perfusion with a hyperosmolar citrate solution. Sulfide (or vehicle treatment) was applied as 0.5 mM NaHS infused 10 min prior and during reperfusion in an in vitro perfusion system.	Renal blood flow and renal function (measured as creatinine clearance, fractional excretion of sodium and urine output) was improved in the sulfide group. Sulfide treatment also resulted in reduced isoprostane and NO levels. No significant differences were observed in histological parameters between groups.	Hosgood and Nicholson, 2010.
Liver	Cold storage of rat livers in Wisconsin solution for 48 h, in the presence or absence of the sulfide donor diallyl disulfide (3.4 mM), followed by perfusion in an isolated constant-pressure perfusion system.	Hepatic clearance (bromosulfophthalein depuration) was enhanced by sulfide treatment; most other parameters (vascular resistance, oxygen consumption, LDH release as an index of cell injury) were unaffected by sulfide.	Balaban et al., 2011.
Cutaneous tissue	In vitro model of cutaneous tissue transplantation: endothelial cells and fibroblasts exposed to hypoxia or anoxia for 24 h, followed by 6 h of normoxia, in the absence or presence of NaHS (10 μM-1 mM).	Sulfide reduced apoptotic index (percentage of TUNEL-positive cells).	Henderson et al., 2010.
Stem cells	In vitro model of stem cell transplantation: rat mesenchymal stem cells exposed to hypoxia or anoxia for 6 h, in the absence or presence of NaHS (200 μM), followed by intramyocardial injection of stem cells and measurement of cardiac function in an ischaemia/reperfusion model in the rat.	Sulfide reduced hypoxia-induced stem cell apoptosis and enhanced donor cell survival in the heart after intramyocardial injection, resulting in improved cardiac contractility. Sulfide treatment was associated with increased Akt, Erk and GSK-3β activation in the stem cells, which has been suggested to contribute to the functional changes observed in vivo.	Xie et al., 2012.