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ToxSci Advance Access published online on March 2, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi139
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Toxicological Sciences © The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received December 7, 2004
Accepted February 13, 2005

Respiratory Toxicology

CO inhalation at dose corresponding to tobacco smoke worsens cardiac remodeling after experimental myocardial infarction in rats

Alain Mirza 1, Véronique Eder 2, Gaël Y Rochefort 2, Jean-Marc Hyvelin 3, Marie Christine Machet 1, Laurent Fauchier 1, and Pierre Bonnet 2*

1 Laboratoire de Physiopathologie de la Paroi Arterielle (LABPART)
2 Laboratoire de Physiopathologie de la Paroi Arterielle (LABPART); Institut Federatif de Recherche 135, Imagerie et Exploration Fonctionnelle
3 Department of Physiology, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland

* To whom correspondence should be addressed.
Pierre Bonnet, E-mail: Bonnet{at}med.univ-tours.fr


  Abstract

Objective: We hypothesized that inhalation of Carbon Monoxide (CO) (500 ppm), similar to that in tobacco smoke, disturbs the cardiovascular adaptation after myocardial infarction by increasing remodeling. Methods: Four groups of rats were assessed. Two groups had myocardial infarction induced by the ligation of the left coronary artery: the first group was exposed to air (Infarcted air group, N=12) and the second was exposed to CO (Infarcted CO group, N=11). They were compared to 2 sham-operated rats, a control air group (N=10) and a control CO group (N=7) exposed (3 weeks) to CO. Results: Aerobic endurance capacity was assessed in both the infarct CO and infarct air group (endurance capacity = 0.043 ± 0.006 m.min-1.g-1 vs. 0.042 ± 0.005 m.min-1.g-1; NS). In the infarcted CO group compared to the infarcted air group, the dilatation of the left ventricle observed 3 weeks after infarction was increased, left ventricular diastolic (LVD) diameter (D)=9±0.4 vs. 7±0.4 mm, p <0.05 and left ventricular systolic (LVS) diameter (D)= 6±0.6 vs. 4.1±0.4, p<0.05) and the diastolic posterior wall thickness was augmented (posterior wall diastolic thickness =1.7±0.1 vs. 1.3±0.1 mm, p<0.05). Hemodynamic pressure measurements in both ventricles and pulmonary artery showed elevated diastolic pressure after CO exposure compared to air exposure (LVD Pressure= 32±1.6 vs.19±2.3 mmHg, p<0.05; Right Ventricular Diastolic Pressure = 16±1.6 vs. 8.6±1.6 mm Hg, p<0.05; Pulmonary arterial pressure in diastole (PAD)= 27±1.6 vs. 20±2.3 mm Hg, p<0.05). In the infarcted CO group, the infarct size increased. Echocardiography and histology showed hypertrophy of the controlateral wall similar to that observed in the non-infarcted control CO group. Conclusion: Chronic CO inhalation worsens heart failure in rats with myocardial infarction by an increase in the infarct size and hypertrophy remodeling.

Keywords: remodeling; heart failure; infarction.
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