Tags

Type your tag names separated by a space and hit enter

H2S concentrations in the heart after acute H2S administration: methodological and physiological considerations.
Am J Physiol Heart Circ Physiol 2016; 311(6):H1445-H1458AJ

Abstract

In this study, we have tried to characterize the limits of the approach typically used to determine H2S concentrations in the heart based on the amount of H2S evaporating from heart homogenates-spontaneously, after reaction with a strong reducing agent, or in a very acidic solution. Heart homogenates were prepared from male rats in control conditions or after H2S infusion induced a transient cardiogenic shock (CS) or cardiac asystole (CA). Using a method of determination of gaseous H2S with a detection limit of 0.2 nmol, we found that the process of homogenization could lead to a total disappearance of free H2S unless performed in alkaline conditions. Yet, after restoration of neutral pH, free H2S concentration from samples processed in alkaline and nonalkaline milieus were similar and averaged ∼0.2-0.4 nmol/g in both control and CS homogenate hearts and up to 100 nmol/g in the CA group. No additional H2S was released from control, CS, or CA hearts by using the reducing agent tris(2-carboxyethyl)phosphine or a strong acidic solution (pH < 2) to "free" H2S from combined pools. Of note, the reducing agent DTT produced a significant sulfide artifact and was not used. These data suggest that 1) free H2S found in heart homogenates is not a reflection of H2S present in a "living" heart and 2) the pool of combined sulfides, released in a strong reducing or acidic milieu, does not increase in the heart in a measurable manner even after toxic exposure to sulfide.

Authors+Show Affiliations

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Pennsylvania State University, College of Medicine, Hershey, Pennsylvania.Division of Pulmonary and Critical Care Medicine, Department of Medicine, Pennsylvania State University, College of Medicine, Hershey, Pennsylvania phaouzi@hmc.psu.edu.

Pub Type(s)

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

Language

eng

PubMed ID

27638880

Citation

Sonobe, Takashi, and Philippe Haouzi. "H2S Concentrations in the Heart After Acute H2S Administration: Methodological and Physiological Considerations." American Journal of Physiology. Heart and Circulatory Physiology, vol. 311, no. 6, 2016, pp. H1445-H1458.
Sonobe T, Haouzi P. H2S concentrations in the heart after acute H2S administration: methodological and physiological considerations. Am J Physiol Heart Circ Physiol. 2016;311(6):H1445-H1458.
Sonobe, T., & Haouzi, P. (2016). H2S concentrations in the heart after acute H2S administration: methodological and physiological considerations. American Journal of Physiology. Heart and Circulatory Physiology, 311(6), pp. H1445-H1458. doi:10.1152/ajpheart.00464.2016.
Sonobe T, Haouzi P. H2S Concentrations in the Heart After Acute H2S Administration: Methodological and Physiological Considerations. Am J Physiol Heart Circ Physiol. 2016 12 1;311(6):H1445-H1458. PubMed PMID: 27638880.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - H2S concentrations in the heart after acute H2S administration: methodological and physiological considerations. AU - Sonobe,Takashi, AU - Haouzi,Philippe, Y1 - 2016/09/16/ PY - 2016/06/29/received PY - 2016/09/15/accepted PY - 2016/9/18/pubmed PY - 2017/6/27/medline PY - 2016/9/18/entrez KW - H2S intoxication KW - acid-labile sulfide KW - protein S-sulfuration SP - H1445 EP - H1458 JF - American journal of physiology. Heart and circulatory physiology JO - Am. J. Physiol. Heart Circ. Physiol. VL - 311 IS - 6 N2 - In this study, we have tried to characterize the limits of the approach typically used to determine H2S concentrations in the heart based on the amount of H2S evaporating from heart homogenates-spontaneously, after reaction with a strong reducing agent, or in a very acidic solution. Heart homogenates were prepared from male rats in control conditions or after H2S infusion induced a transient cardiogenic shock (CS) or cardiac asystole (CA). Using a method of determination of gaseous H2S with a detection limit of 0.2 nmol, we found that the process of homogenization could lead to a total disappearance of free H2S unless performed in alkaline conditions. Yet, after restoration of neutral pH, free H2S concentration from samples processed in alkaline and nonalkaline milieus were similar and averaged ∼0.2-0.4 nmol/g in both control and CS homogenate hearts and up to 100 nmol/g in the CA group. No additional H2S was released from control, CS, or CA hearts by using the reducing agent tris(2-carboxyethyl)phosphine or a strong acidic solution (pH < 2) to "free" H2S from combined pools. Of note, the reducing agent DTT produced a significant sulfide artifact and was not used. These data suggest that 1) free H2S found in heart homogenates is not a reflection of H2S present in a "living" heart and 2) the pool of combined sulfides, released in a strong reducing or acidic milieu, does not increase in the heart in a measurable manner even after toxic exposure to sulfide. SN - 1522-1539 UR - https://www.unboundmedicine.com/medline/citation/27638880/H2S_concentrations_in_the_heart_after_acute_H2S_administration:_methodological_and_physiological_considerations_ L2 - http://www.physiology.org/doi/full/10.1152/ajpheart.00464.2016?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -