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

Hydrogen sulfide (H₂S) intoxication produces a rapid cardio-circulatory failure leading to cardiac arrest. In non-lethal forms of sulfide exposure, the presence of a circulatory shock is associated with long-term neurological sequelae. Our aim was to clarify the mechanisms of H₂S-induced circulatory failure. In anesthetized, paralyzed, and mechanically ventilated rats, cardiac output, arterial pressure and ventricular pressures were determined while NaHS was infused to increase arterial concentration of soluble H₂S (CgH₂S) from undetectable to levels leading to circulatory failure. Compared to control/saline infusion, blood pressure started to decrease significantly along with a modest drop in peripheral vascular resistance (−19 ± 5 %, P < 0.01), when CgH₂S reached about 1 μM. As CgH₂S exceeded 2–3 μM, parameters of ventricular contractility diminished with no further reduction in peripheral resistance. Whenever H₂S exposure was maintained at a higher level (CgH₂S over 7 μM), a severe depression of cardiac contractility was observed, leading to asystole within minutes, but with no evidence of peripheral vasoplegia. The immediate and long-term neurological effects of specifically counteracting sulfide-induced cardiac contractility depression following H₂S exposure remain to be investigated.