Peracute toxic effects of inhaled hydrogen sulfide and injected sodium hydrosulfide on the lungs of rats

H2S induced coma and cardiogenic shock in the rat: Effects of phenothiazinium chromophores

“…In our experience, pulmonary edema will only be present if the animal is resuscitated by CPR maneuvers and epinephrine injection—this is also true in larger mammals. 2 This difference between the effects of inhaled and infused sulfide has already been described by Lopez et al, 80 who found very similar results, that is, lack of pulmonary edema during lethal infusion of H 2 S, in contrast to inhaled exposure. In addition, we found that the peak values of alveolar H 2 S for 10 min were not high enough to produce any significant lung toxicity, since a similar rat model would require at least 400 ppm for one hour to produce a pulmonary edema.…”

Sulfide Intoxication-Induced Circulatory Failure is Mediated by a Depression in Cardiac Contractility

“…Certainly the toxicity of sulfide towards the lungs and the upper-airways [38, 39] is expected to be blunted, at any given level of sulfide in the blood, if sulfides are infused rather than inhaled [40]. However, as soon as H 2 S reaches the blood, the original site of diffusion, whether the alveolar regions to or a direct venous infusion, is not going to affect the distribution of the various pools of sulfide in the blood and the concentration of H 2 S in the tissues (see above paragraph and ref for discussion [9, 10, 35]).…”

“…The interest of using these compounds in investigating sulfide toxicity is yet to be established. Indeed, a slow H 2 S releasing compound [41] is not faithful to a real life scenario created by an exposure to toxic levels of H 2 S, in keeping with the very fast kinetics of H 2 S toxicity (coma, respiratory arrest or circulatory failure), which can be produced within seconds during inhalation of H 2 S or infusion of solution of sulfide obtained from NaHS [40, 42]. Perhaps more importantly, whenever GYY4137 “releases” H 2 S, the latter will, for most of it, be immediately transformed into HS - along with the creation of a pool of sulfides combined to proteins in various ways, including in sulfhydration form [15, 43], just like any sources of exogenous or endogenous H 2 S. For all intends and purposes, the reduction in left cardiac contractility during H 2 S infusion that we are reporting in the present study appears to be an early sign of sulfide toxicity and thus represents a relevant mechanism responsible of the circulatory failure that occur very early during sulfide inhalation.…”

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

“…TBSA produces a large systemic inflammatory reaction characterized by leukocyte activation and plasma leakage in the microvasculature of tissues and organs remote from the wound. The degree of inflammatory response correlates directly with the percentage of TBSA burn [58,59]. In mice subjected to 30% TBSA burn injury [56,57], significantly elevated plasma and hepatic H 2 S levels with a concomitant increase in liver and lung expression of CSE were observed 8 h post-burn injury.…”

“…H 2 S gas inhalation is well known to induce substantive pulmonary edema characterized by extensive eosinophilic extravasation into the bronchoalveolar space and fibrinocellular alveolitis [59,60], suggesting modulation of endogenous H 2 S synthesis could represent a novel pathway in chronic inflammatory lung disease. Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation throughout the airways, parenchymal and pulmonary vasculature, resulting in substantial airflow obstruction.…”