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Sulfide Intoxication-Induced Circulatory Failure is Mediated by a Depression in Cardiac Contractility.
Cardiovasc Toxicol 2016; 16(1):67-78CT

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.

Authors+Show Affiliations

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Pennsylvania State University, College of Medicine, 500 University Drive, H041, Hershey, PA, 17033, USA.Division of Pulmonary and Critical Care Medicine, Department of Medicine, Pennsylvania State University, College of Medicine, 500 University Drive, H041, Hershey, PA, 17033, USA. phaouzi@hmc.psu.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

25616319

Citation

Sonobe, Takashi, and Philippe Haouzi. "Sulfide Intoxication-Induced Circulatory Failure Is Mediated By a Depression in Cardiac Contractility." Cardiovascular Toxicology, vol. 16, no. 1, 2016, pp. 67-78.
Sonobe T, Haouzi P. Sulfide Intoxication-Induced Circulatory Failure is Mediated by a Depression in Cardiac Contractility. Cardiovasc Toxicol. 2016;16(1):67-78.
Sonobe, T., & Haouzi, P. (2016). Sulfide Intoxication-Induced Circulatory Failure is Mediated by a Depression in Cardiac Contractility. Cardiovascular Toxicology, 16(1), pp. 67-78. doi:10.1007/s12012-015-9309-z.
Sonobe T, Haouzi P. Sulfide Intoxication-Induced Circulatory Failure Is Mediated By a Depression in Cardiac Contractility. Cardiovasc Toxicol. 2016;16(1):67-78. PubMed PMID: 25616319.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sulfide Intoxication-Induced Circulatory Failure is Mediated by a Depression in Cardiac Contractility. AU - Sonobe,Takashi, AU - Haouzi,Philippe, PY - 2015/1/25/entrez PY - 2015/1/27/pubmed PY - 2016/10/1/medline KW - Cardiac toxicity KW - H2S KW - Vascular blood flow KW - Vasodilation SP - 67 EP - 78 JF - Cardiovascular toxicology JO - Cardiovasc. Toxicol. VL - 16 IS - 1 N2 - 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. SN - 1559-0259 UR - https://www.unboundmedicine.com/medline/citation/25616319/Sulfide_Intoxication_Induced_Circulatory_Failure_is_Mediated_by_a_Depression_in_Cardiac_Contractility_ L2 - https://dx.doi.org/10.1007/s12012-015-9309-z DB - PRIME DP - Unbound Medicine ER -