Detection of exhaled hydrogen sulphide gas in rats exposed to intravenous sodium sulphide

Insko, Michael A; Deckwerth, Thomas L.; Hill, Paul; Toombs, Christopher F.; Szabó, Csaba

doi:10.1111/j.1476-5381.2009.00248.x

Cited by 70 publications

(63 citation statements)

References 47 publications

(85 reference statements)

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“…This approach, which differs from traditional amperometry, relies on a certain number of prerequisites and limits. We found that the RM17-1000b hydrogen sulfide detector, which was previously used to estimate the rate of elimination of H 2 S by the lungs (29), is sensitive to change in humidity, which would require it to re-zero when connected to expired gas unless dry gas is used. Second, the sampling flow of these analyzers is high (around 0.5 l/min, which is about 2 times the minute ventilation of a rat) but does fluctuate around its set value.…”

Section: What Was Measured In the Blood?mentioning

confidence: 99%

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

Klingerman

Trushin

Prokopczyk

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

129

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Klingerman CM, Trushin N, Prokopczyk B, Haouzi P. 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 305: R630 -R638, 2013. First published July 31, 2013; doi:10.1152/ajpregu.00218.2013.-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, H 2S 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, H 2S was undetectable in the blood in its soluble form in baseline conditions, while CMBBH 2S averaged 0.7 Ϯ 0.5 M. During NaHS infusion, H 2S was primarily present in nonsoluble form in the arterial blood: CMBBH 2S was about 50 times higher than CgH 2S at the lowest levels of exposure and 5 or 6 times at the levels wherein fatal apnea occurred. CgH 2S averaged only 1.1 Ϯ 0.7 M when breathing increased, corresponding to a CMBBH 2S of 11.1 Ϯ 5.4 M. Apnea occurred at CgH 2S above 5.1 M and CMBBH2S above 25.4 M. At the cessation of exposure, CMBBH 2S 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 H 2S and for testing antidotes against its deadly effects.

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Section: What Was Measured In the Blood?mentioning

confidence: 99%

“…In the current study, following experiments from Insko et al (29) and Wintner et al (54), we infused H 2 S intravenously in the form of NaHS to spontaneously breathing, urethane-anesthetized rats. We increased the infusion rate gradually until an apnea occurred ("lethal" exposure).…”

mentioning

confidence: 99%

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

Klingerman

Trushin

Prokopczyk

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

129

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“…In contrast, patients with exacerbations of COPD have significantly decreased levels of serum H 2 S. Thus, levels of endogenous H 2 S may represent a potential indicator of COPD severity. [9][10][11] However, the relationship between levels of exhaled H 2 S and airway or systemic inflammation has not yet been determined. Recently, the analysis of signaling molecules present in exhaled air has become a popular technique for noninvasive assessment of airway inflammation.…”

Section: Introductionmentioning

confidence: 99%

Exhaled Hydrogen Sulfide Predicts Airway Inflammation Phenotype in COPD

et al. 2014

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BACKGROUND: The role of exhaled H 2 S as a marker of airway inflammation and its relationship with COPD severity remain to be determined. METHODS: Airway inflammation was classified in 77 COPD subjects based on the presence of inflammatory cells in induced sputum. We investigated the association between disease phenotype and exhaled H 2 S, lung function, and plasma levels of several inflammatory factors, including tumor necrosis factor alpha, interleukin-8, and leukotriene B 4 . RESULTS: In total, 33.77% of enrolled COPD subjects were diagnosed with eosinophilia. These subjects had a longer disease course, smoked fewer cigarettes, and experienced more frequent exacerbation events before study enrollment. However, they also had worse lung function and larger residual volume, they demonstrated greater changes in FEV 1 following bronchodilator inhalation. Although levels of plasma inflammatory factors did not significantly differ between subjects with and without eosinophilia, subjects without eosinophilia had significantly higher levels of exhaled H 2 S (9.19 ؎ 2.74 vs 7.24 ؎ 1.68 parts per billion, P ‫؍‬ .01). Furthermore, exhaled H 2 S levels were negatively correlated with induced sputum eosinophils (r ‫؍‬ ؊0.45, P ‫؍‬ .05), and positively correlated with inspiratory capacity in COPD subjects (r ‫؍‬ 0.51, P ‫؍‬ .026), but did not correlate significantly with plasma inflammatory factors. A cut-off value of 7.10 parts per billion of exhaled H 2 S predicted a non-eosinophilic phenotype with 68.6% sensitivity and 77.9% specificity. CONCLUSIONS: Exhaled levels of H 2 S were lower in subjects with eosinophilia. Increased levels of exhaled H 2 S predicted a non-eosinophilic phenotype in our study population. Key words: chronic obstructive pulmonary disease; airway inflammation phenotype; eosinophilia; hydrogen sulfide. [Respir Care 2015;60(2):251-258.

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“…In in vivo conditions (37°C, pH ϳ7.4), H 2 S is predicted to exist as 14% free H 2 S gas, 86% HS Ϫ , and trace levels of S 2Ϫ (96,153). Limitations to measuring H 2 S include 1) free H 2 S has a short half-life, ranging from 12 to 300 s in various species, and 2) detection methods may release bound sulfur from proteins, resulting in increased H 2 S concentrations (61,96,142,153).…”

mentioning

confidence: 99%

“…Although the intermediate pathways involved in the oxidation of H 2 S are not completely understood, sulfate is the primary by-product of sulfide catabolism, which may be excreted in the urine and feces (63,69,90). An additional pathway for excretion of H 2 S may include expiration by the lungs (61,142). H 2 S may be scavenged by disulfide-containing molecules and red blood cells, where H 2 S binds to methemoglobin forming sulfhemoglobin, which is oxidized to thiosulfate (147).…”

mentioning

confidence: 99%