Beneficial effect of a hydrogen sulphide donor (sodium sulphide) in an ovine model of burn- and smoke-induced acute lung injury

Aimalohi Esechie, Perenlei Enkhbaatar, Daniel L. Traber, Collette Jonkam, Matthias Lange, Atsumori Hamahata, Clarisse Djukom, Elbert B. Whorton, Hal K. Hawkins, Lillian D. Traber, Csaba Szabo

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Background and purpose: The present study investigated whether the pathophysiological changes induced by burn and smoke inhalation are modulated by parenteral administration of Na 2S, a H 2S donor. Experimental approach: The study used a total of 16 chronically instrumented, adult female sheep. Na 2S was administered 1 h post injury, as a bolus injection at a dose of 0.5 mg·kg -1 and subsequently, as a continuous infusion at a rate of 0.2 mg·kg -1·h -1 for 24 h. Cardiopulmonary variables (mean arterial and pulmonary arterial blood pressure, cardiac output, ventricular stroke work index, vascular resistance) and arterial and mixed venous blood gases were measured. Lung wet-to-dry ratio and myeloperoxidase content and protein oxidation and nitration were also measured. In addition, lung inducible nitric oxide synthase expression and cytochrome c were measured in lung homogenates via Western blotting and enzyme-linked immunosorbent assay (elisa) respectively. Key results: The H 2S donor decreased mortality during the 96 h experimental period, improved pulmonary gas exchange and lowered further increase in inspiratory pressure and fluid accumulation associated with burn- and smoke-induced acute lung injury. Further, the H 2S donor treatment reduced the presence of protein oxidation and 3-nitrotyrosine formation following burn and smoke inhalation injury. Conclusions and implications: Parenteral administration of the H 2S donor ameliorated the pulmonary pathophysiological changes associated with burn- and smoke-induced acute lung injury. Based on the effect of H 2S observed in this clinically relevant model of disease, we propose that treatment with H 2S or its donors may represent a potential therapeutic strategy in managing patients with acute lung injury.

Original languageEnglish (US)
Pages (from-to)1442-1453
Number of pages12
JournalBritish Journal of Pharmacology
Volume158
Issue number6
DOIs
StatePublished - Nov 2009

Fingerprint

Hydrogen Sulfide
Acute Lung Injury
Burns
Smoke
Sheep
Tissue Donors
Lung
Inhalation Burns
Smoke Inhalation Injury
Pulmonary Gas Exchange
Nitric Oxide Synthase Type II
Pulmonary Edema
Cytochromes c
Cardiac Output
Vascular Resistance
Peroxidase
Arterial Pressure
Proteins
Therapeutics
Gases

Keywords

  • Acute lung injury
  • Hydrogen sulphide
  • Protein oxidation
  • Sheep
  • Smoke inhalation

ASJC Scopus subject areas

  • Pharmacology

Cite this

Beneficial effect of a hydrogen sulphide donor (sodium sulphide) in an ovine model of burn- and smoke-induced acute lung injury. / Esechie, Aimalohi; Enkhbaatar, Perenlei; Traber, Daniel L.; Jonkam, Collette; Lange, Matthias; Hamahata, Atsumori; Djukom, Clarisse; Whorton, Elbert B.; Hawkins, Hal K.; Traber, Lillian D.; Szabo, Csaba.

In: British Journal of Pharmacology, Vol. 158, No. 6, 11.2009, p. 1442-1453.

Research output: Contribution to journalArticle

Esechie, Aimalohi ; Enkhbaatar, Perenlei ; Traber, Daniel L. ; Jonkam, Collette ; Lange, Matthias ; Hamahata, Atsumori ; Djukom, Clarisse ; Whorton, Elbert B. ; Hawkins, Hal K. ; Traber, Lillian D. ; Szabo, Csaba. / Beneficial effect of a hydrogen sulphide donor (sodium sulphide) in an ovine model of burn- and smoke-induced acute lung injury. In: British Journal of Pharmacology. 2009 ; Vol. 158, No. 6. pp. 1442-1453.
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AU - Esechie, Aimalohi

AU - Enkhbaatar, Perenlei

AU - Traber, Daniel L.

AU - Jonkam, Collette

AU - Lange, Matthias

AU - Hamahata, Atsumori

AU - Djukom, Clarisse

AU - Whorton, Elbert B.

AU - Hawkins, Hal K.

AU - Traber, Lillian D.

AU - Szabo, Csaba

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N2 - Background and purpose: The present study investigated whether the pathophysiological changes induced by burn and smoke inhalation are modulated by parenteral administration of Na 2S, a H 2S donor. Experimental approach: The study used a total of 16 chronically instrumented, adult female sheep. Na 2S was administered 1 h post injury, as a bolus injection at a dose of 0.5 mg·kg -1 and subsequently, as a continuous infusion at a rate of 0.2 mg·kg -1·h -1 for 24 h. Cardiopulmonary variables (mean arterial and pulmonary arterial blood pressure, cardiac output, ventricular stroke work index, vascular resistance) and arterial and mixed venous blood gases were measured. Lung wet-to-dry ratio and myeloperoxidase content and protein oxidation and nitration were also measured. In addition, lung inducible nitric oxide synthase expression and cytochrome c were measured in lung homogenates via Western blotting and enzyme-linked immunosorbent assay (elisa) respectively. Key results: The H 2S donor decreased mortality during the 96 h experimental period, improved pulmonary gas exchange and lowered further increase in inspiratory pressure and fluid accumulation associated with burn- and smoke-induced acute lung injury. Further, the H 2S donor treatment reduced the presence of protein oxidation and 3-nitrotyrosine formation following burn and smoke inhalation injury. Conclusions and implications: Parenteral administration of the H 2S donor ameliorated the pulmonary pathophysiological changes associated with burn- and smoke-induced acute lung injury. Based on the effect of H 2S observed in this clinically relevant model of disease, we propose that treatment with H 2S or its donors may represent a potential therapeutic strategy in managing patients with acute lung injury.

AB - Background and purpose: The present study investigated whether the pathophysiological changes induced by burn and smoke inhalation are modulated by parenteral administration of Na 2S, a H 2S donor. Experimental approach: The study used a total of 16 chronically instrumented, adult female sheep. Na 2S was administered 1 h post injury, as a bolus injection at a dose of 0.5 mg·kg -1 and subsequently, as a continuous infusion at a rate of 0.2 mg·kg -1·h -1 for 24 h. Cardiopulmonary variables (mean arterial and pulmonary arterial blood pressure, cardiac output, ventricular stroke work index, vascular resistance) and arterial and mixed venous blood gases were measured. Lung wet-to-dry ratio and myeloperoxidase content and protein oxidation and nitration were also measured. In addition, lung inducible nitric oxide synthase expression and cytochrome c were measured in lung homogenates via Western blotting and enzyme-linked immunosorbent assay (elisa) respectively. Key results: The H 2S donor decreased mortality during the 96 h experimental period, improved pulmonary gas exchange and lowered further increase in inspiratory pressure and fluid accumulation associated with burn- and smoke-induced acute lung injury. Further, the H 2S donor treatment reduced the presence of protein oxidation and 3-nitrotyrosine formation following burn and smoke inhalation injury. Conclusions and implications: Parenteral administration of the H 2S donor ameliorated the pulmonary pathophysiological changes associated with burn- and smoke-induced acute lung injury. Based on the effect of H 2S observed in this clinically relevant model of disease, we propose that treatment with H 2S or its donors may represent a potential therapeutic strategy in managing patients with acute lung injury.

KW - Acute lung injury

KW - Hydrogen sulphide

KW - Protein oxidation

KW - Sheep

KW - Smoke inhalation

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