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H2S concentrations in the arterial blood during H2S administration in relation to its toxicity and effects on breathing.

Abstract

Our aim was to establish in spontaneously breathing urethane-anesthetized rats, the relationship between the concentrations of H2S transported in the blood and the corresponding clinical manifestations, i.e., breathing stimulation and inhibition, during and following infusion of NaHS at increasing rates. The gaseous concentration of H2S (CgH2S, one-third of the total soluble form) was computed from the continuous determination of H2S partial pressure in the alveolar gas, while H2S, both dissolved and combined to hemoglobin, was measured at specific time points by sulfide complexation with monobromobimane (CMBBH2S). We found that using a potent reducing agent in vitro, H2S added to the whole blood had little interaction with the plasma proteins, as sulfide appeared to be primarily combined and then oxidized by hemoglobin. In vivo, H2S was undetectable in the blood in its soluble form in baseline conditions, while CMBBH2S averaged 0.7 ± 0.5 μM. During NaHS infusion, H2S was primarily present in nonsoluble form in the arterial blood: CMBBH2S was about 50 times higher than CgH2S at the lowest levels of exposure and 5 or 6 times at the levels wherein fatal apnea occurred. CgH2S averaged only 1.1 ± 0.7 μM when breathing increased, corresponding to a CMBBH2S of 11.1 ± 5.4 μM. Apnea occurred at CgH2S above 5.1 μM and CMBBH2S above 25.4 μM. At the cessation of exposure, CMBBH2S remained elevated, at about 3 times above baseline for at least 15 min. These data provide a frame of reference for studying the putative effects of endogenous H2S and for testing antidotes against its deadly effects.

Authors+Show Affiliations

Department of Medicine, Division of Pulmonary and Critical Care Medicine, Penn State University College of Medicine, Hershey, Pennsylvania; and.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

23904109

Citation

Klingerman, Candice M., et al. "H2S Concentrations in the Arterial Blood During H2S Administration in Relation to Its Toxicity and Effects On Breathing." American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, vol. 305, no. 6, 2013, pp. R630-8.
Klingerman CM, Trushin N, Prokopczyk B, et al. H2S concentrations in the arterial blood during H2S administration in relation to its toxicity and effects on breathing. Am J Physiol Regul Integr Comp Physiol. 2013;305(6):R630-8.
Klingerman, C. M., Trushin, N., Prokopczyk, B., & Haouzi, P. (2013). H2S concentrations in the arterial blood during H2S administration in relation to its toxicity and effects on breathing. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 305(6), pp. R630-8. doi:10.1152/ajpregu.00218.2013.
Klingerman CM, et al. H2S Concentrations in the Arterial Blood During H2S Administration in Relation to Its Toxicity and Effects On Breathing. Am J Physiol Regul Integr Comp Physiol. 2013 Sep 15;305(6):R630-8. PubMed PMID: 23904109.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - H2S concentrations in the arterial blood during H2S administration in relation to its toxicity and effects on breathing. AU - Klingerman,Candice M, AU - Trushin,Neil, AU - Prokopczyk,Bogdan, AU - Haouzi,Philippe, Y1 - 2013/07/31/ PY - 2013/8/2/entrez PY - 2013/8/2/pubmed PY - 2013/11/6/medline KW - control of respiration KW - hydrogen sulfide KW - toxicity SP - R630 EP - 8 JF - American journal of physiology. Regulatory, integrative and comparative physiology JO - Am. J. Physiol. Regul. Integr. Comp. Physiol. VL - 305 IS - 6 N2 - Our aim was to establish in spontaneously breathing urethane-anesthetized rats, the relationship between the concentrations of H2S transported in the blood and the corresponding clinical manifestations, i.e., breathing stimulation and inhibition, during and following infusion of NaHS at increasing rates. The gaseous concentration of H2S (CgH2S, one-third of the total soluble form) was computed from the continuous determination of H2S partial pressure in the alveolar gas, while H2S, both dissolved and combined to hemoglobin, was measured at specific time points by sulfide complexation with monobromobimane (CMBBH2S). We found that using a potent reducing agent in vitro, H2S added to the whole blood had little interaction with the plasma proteins, as sulfide appeared to be primarily combined and then oxidized by hemoglobin. In vivo, H2S was undetectable in the blood in its soluble form in baseline conditions, while CMBBH2S averaged 0.7 ± 0.5 μM. During NaHS infusion, H2S was primarily present in nonsoluble form in the arterial blood: CMBBH2S was about 50 times higher than CgH2S at the lowest levels of exposure and 5 or 6 times at the levels wherein fatal apnea occurred. CgH2S averaged only 1.1 ± 0.7 μM when breathing increased, corresponding to a CMBBH2S of 11.1 ± 5.4 μM. Apnea occurred at CgH2S above 5.1 μM and CMBBH2S above 25.4 μM. At the cessation of exposure, CMBBH2S remained elevated, at about 3 times above baseline for at least 15 min. These data provide a frame of reference for studying the putative effects of endogenous H2S and for testing antidotes against its deadly effects. SN - 1522-1490 UR - https://www.unboundmedicine.com/medline/citation/23904109/H2S_concentrations_in_the_arterial_blood_during_H2S_administration_in_relation_to_its_toxicity_and_effects_on_breathing_ L2 - http://www.physiology.org/doi/full/10.1152/ajpregu.00218.2013?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -