“…For example: lethal hypoxia [3], ischemia/reperfusion (I/R)-injury [4–30], cardiac arrest [31–36], hemorrhage and resuscitation [37–45], acute lung injury resulting from blunt chest trauma [46,47] and/or injurious mechanical ventilation [48–50], as well as systemic inflammation resulting from endotoxin injection [51–59], acute pancreatitis [60–63], polymicrobial sepsis [64–70], and/or burn injury [71–73]. While the beneficial effect of exogenous H 2 S supplementation and maintaining endogenous H 2 S production, respectively, are well-established in I/R injury, equivocal results were reported after cardiac arrest, hemorrhage and resuscitation, and, in particular, in sepsis: inhaling gaseous H 2 S [33,44,48,50,53,54,65], the injection of the sulfide-containing salts NaSH [31,39,49,51,59,63,64,66–71,120] and Na 2 S [32,34–38,41,42,44,47,48,72,73] or the slow-releasing H 2 S donor GYY4137 [55] as well as of inhibitors of H 2 S production [43,45,58–60,62,63,67–71,120] were associated with attenuation of shock-related organ dysfunction.…”