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J Investig Med. 2004 Dec;52(8):523-30. doi: 10.1136/jim-52-08-24.

Effects of carbon monoxide poisoning on neutrophil responses in patients treated with hyperbaric oxygen.

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Department of Anesthesia and Intensive Care Medicine, Karolinska University Hospital, Solna, Sweden.



Carbon monoxide (CO) poisoning can cause tissue injury. Neutrophil granulocytes have been proposed to contribute to the injury, which may be ameliorated by hyperbaric oxygen (HBO2) treatment. We sought to assess the relationship between acute CO poisoning and blood neutrophil count, plasma cytokine, and cortisol responses, as well as the mechanism behind the observed beneficiary effects of HBO2 treatment.


Eight patients (age 26-82 years) with severe acute CO poisoning were enrolled, concomitant with eight healthy controls (age 27-42 years), in a prospective, controlled, clinical study. The patients were given three HBO2 treatments (2.8 atmospheres absolute, 100 minutes) within the first 24 hours. The controls were given identical simultaneous HBO2 treatments. Venous blood samples were taken before and after each treatment.


At the start of the HBO2 treatment, patients displayed significantly higher blood neutrophil counts (p < .0001) and plasma cortisol levels (p = .020) than controls, but the two groups had similar values for interleukin-8, granulocyte colony-stimulating factor (G-CSF), neutrophil H2O2 generation, and CD16 and CD18 surface expression. During the observation time, neutrophil H2O2 accumulation declined in patients and in controls (p = .031), whereas the up-regulation of CD18 expression increased (p = .002) in both groups. Moreover, G-CSF levels became significantly higher in patients than in controls (p = .015). G-CSF levels also correlated significantly with neutrophil counts.


CO poisoning was associated with discrete changes of blood neutrophil counts, cortisol, and G-CSF plasma concentrations. HBO2 treatment modulated neutrophil generation of H2O2 and surface expression of CD18. These changes may be part of the cascade of events leading to the sequelae of CO poisoning and their attenuation by HBO2.

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