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

Takashi Sonobe, Philippe Haouzi

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)67-78
Number of pages12
JournalCardiovascular toxicology
Volume16
Issue number1
DOIs
StatePublished - Jan 1 2016

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Toxicology
  • Cardiology and Cardiovascular Medicine

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