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 language | English (US) |
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Pages (from-to) | 754-758 |
Number of pages | 5 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 311 |
Issue number | 3 |
DOIs | |
State | Published - 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