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Published ahead of print on May 11, 2006, doi:10.1164/rccm.200601-117OC

Am. J. Respir. Crit. Care Med., Volume 174, Number 3, August 2006, 320-325

A more recent version of this article appeared on August 1, 2006
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Submitted on January 26, 2006
Accepted on May 5, 2006

Myocardial Dysfunction and Potential Cardiac Hypoxia in Rats Induced by Carbon Monoxide Inhalation

Raphael Favory1, Steve Lancel2, Stephanie Tissier1, Daniel Mathieu3, Brigitte Decoster2, and Remi Neviere2*

1 Intensive Care Unit and Hyperbaric Regional Center, University Hospital of Lille, Lille, France; EA 2689, University Lille 2, Lille, France, 2 EA 2689, University Lille 2, Lille, France; Department of Physiology, University of Lille 2, Faculty of Medicine, Lille, France, 3 Intensive Care Unit and Hyperbaric Regional Center, University Hospital of Lille, Lille, France

* To whom correspondence should be addressed. E-mail: rneviere{at}univ-lille2.fr.

Background: Results from both animal and human being studies provide evidence that inhalation of concentrations of carbon monoxide (CO) at around hundred(s) part per million (ppm) have anti-inflammatory effects. As a different concept, such low levels of CO are incriminated in ischemic heart diseases experienced by cigarette smokers and in some case from air pollution. Although neurological mechanisms have been investigated, the effects of CO on cardiovascular function are still poorly understood. Methods and Results: The effects of carbon monoxide (250 ppm; 90 min) inhalation on myocardial function were investigated in isolated heart of rats sacrificed immediately, 3, 24, 48 and 96 h after CO exposure. CO exposure at 250 ppm resulted in ~11 % arterial carboxy hemoglobin (HbCO) level, which was not associated with changes in mean arterial pressure and heart rate. CO exposure induced coronary perfusion pressure increases, which were associated with endothelium-dependent and endothelium-independent vascular relaxation abnormalities. CO-induced coronary vascular relaxation perturbations were observed in the presence of increased heart contractility. Spontaneous peak to maximal Ca2+-activated left ventricular pressure ratio was markedly increased in CO exposed rats indicating increases in myofilament calcium sensitivity. Heart cGMP/cAMP ratio and myocardial permeabilized fiber respiration (complex IV activity) were reduced in CO exposed rats, which lasted after 48h of reoxygenation in air. Conclusions: These findings support the contention that CO deteriorates heart oxygen supply to utilization with potential myocardial hypoxia via mechanisms including increased oxygen demand due to increased contractility, reduced coronary blood flow reserve and cardiomyocyte respiration inhibition.
Key words: carbon monoxide, endothelium, contractility, cardiomyopathy




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