Carboxyhemoglobin formation following smoke inhalation injury in sheep is interrelated with pulmonary shunt fraction

Martin Westphal, Naoki Morita, Perenlei Enkhbaatar, Kazunori Murakami, Lillian Traber, Daniel Lee Traber

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Carboxyhemoglobin (COHb) formation is triggered by the inducible isoform of heme oxygenase (HO-1) catalyzing carbon monoxide (CO) production through breakdown of heme molecules, exposure to CO or both. In the setting of CO poisoning, COHb is regarded as a reliable marker characterizing both severity of injury and efficacy of treatment strategies. This study was designed as a prospective laboratory experiment to elucidate potential interdependencies between COHb generation, oxygenation, and pulmonary shunt fraction (Qs/Qt) in an ovine model of smoke inhalation injury. Chronically instrumented ewes (n=15) were repeatedly subjected to cotton smoke (4×12 breaths) according to an established protocol. This approach resulted in a progressive increase in COHb formation that was interrelated with the degree of Qs/Qt (P<0.001) and inversely correlated with both arterial and mixed venous HbO2 saturation (r=-0.96 and -0.93). Although the arteriovenous COHb gradient successively decreased over time, COHb determined in venous blood underestimated the arterial content.

Original languageEnglish (US)
Pages (from-to)754-758
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume311
Issue number3
DOIs
StatePublished - Nov 21 2003

Keywords

  • Carbon monoxide poisoning
  • Carboxyhemoglobin
  • Critical illness
  • Heme oxygenase
  • Hypoxic pulmonary vasoconstriction
  • Lung
  • Oxygen saturation
  • Smoke inhalation

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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