Does hydrogen sulfide improve resuscitation via non-hibernatory mechanisms in a porcine shock model?
Administration of H2S in a large-animal model of severe traumatic shock resulted in a significant decrease in resuscitative requirements, decreased metabolic acidosis, and less end-organ histologic injury compared with standard resuscitation. H2S did not induce profound metabolic suppression as seen in rodents, and appears to have alternative mechanisms of action in large animals.
The experimental joint capsule changes in the acute stages of posttraumatic contractures are similar to those in the chronic stages of the process in this model. Thus, it appears that the mechanisms that attenuate the acute stages of the response to injury are circumvented, contributing to a prolonged modulation of myofibroblast numbers, matrix molecules and growth factors, and leading to joint contractures. Thus, in clinical practice, new approaches to prevention of posttraumatic contractures should be implemented as soon as possible.