Meyer J, Prien T, Van Aken H, Bone H G, Waurick R, Theilmeier G, Booke M
Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Westfälische Wilhelms-Universität Münster, Germany.
Biochem Biophys Res Commun. 1998 Mar 6;244(1):230-2. doi: 10.1006/bbrc.1998.8244.
Carbon monoxide is hypothesized to be produced by the enzyme heme oxygenase predominantly in liver and spleen, bound to hemoglobin, and excreted by the lungs. Thus, venous carboxyhemoglobin is expected to be higher or equal to arterial carboxyhemoglobin. Unspecific inflammatory stimuli have been shown to induce heme oxygenase in lung tissue possibly leading to pulmonary carbon monoxide production. Arterial and central venous carboxyhemoglobin levels were measured in critically ill patients on the third day of ICU stay (n = 59) as well as in otherwise healthy humans prior to orthopedic surgery (n = 29). Arterial and central venous carboxyhemoglobin were higher in ICU patients than in healthy humans, respectively. In both groups, arterial carboxyhemoglobin was significantly higher than central venous carboxyhemoglobin. The arteriovenous carboxyhemoglobin differences were similar in both groups. The data suggest (a) increased CO-generation in critical illness and (b) pulmonary CO-production in healthy and critically ill humans.
