Published ahead of print on November 19, 2004, doi:10.1164/rccm.200404-446OC Am. J. Respir. Crit. Care Med., Volume 171, Number 4, February 2005, 354-360 A more recent version of this article appeared on February 15, 2005
Submitted on April 2, 2004 Effects of Carbon Monoxide Inhalation during Experimental Endotoxemia in HumansFlorian B Mayr1,1 Department of Clinical Pharmacology, Medical University Vienna, Vienna, Austria, 2 Department of Medical and Chemical Laboratory Diagnostics, Medical University Vienna, Vienna, Austria, 3 Department of Anesthesiology and General Critical Care Medicine, Medical University Vienna, Vienna, Austria * To whom correspondence should be addressed. E-mail: Bernd.Jilma{at}meduniwien.ac.at.
Recent data show that carbon monoxide (CO) exerts direct anti-inflammatory effects in vitro and in vivo after lipopolysaccharide (LPS) challenge in a mouse model. We hypothesized that CO may act as an anti-inflammatory agent in human endotoxemia. The aim of this trial was to study the effects of CO inhalation on cytokine production during experimental human endotoxemia. The main study was randomized, double-blinded, placebo-controlled two-way crossover in healthy volunteers. Each volunteer inhaled synthetic air (as placebo) and 500 ppm CO for 1 hour in random order with a washout period of 6 weeks and received a 2 ng/kg intravenous bolus of LPS after inhalation. HbCO levels were assessed as a safety parameter. CO inhalation increased HbCO levels from 1.2% [95%CI: 1.0-1.4%] to peak values of 7.0 [CI:6.5-7.7%]. LPS infusion transiently increased plasma concentrations of TNF Key words: CO, endotoxin, TNF, HbCO
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, IL-6 (~150-fold increases), IL-8 as well as IL-1
mRNA levels (~200-fold increase). These LPS-induced changes were not influenced by CO inhalation. Inhalation of 500 ppm CO for 1 hour had no anti-inflammatory effects in a systemic inflammation model in humans as 250 ppm for 1 hour did in rodents.
