CO inhalation at dose corresponding to tobacco smoke worsens cardiac remodeling after experimental myocardial infarction in rats.
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. 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 two sham-operated groups, a control air group (n = 10), and a control CO group (n = 7) exposed (3 weeks) to CO. 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), not significant). 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; 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 mm Hg, 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 contralateral wall similar to that observed in the noninfarcted control CO group. In conclusion, chronic CO inhalation worsens heart failure in rats with myocardial infarction by an increase in the infarct size and hypertrophy remodeling.
Mirza
Alain
A
Laboratoire de Physiopathologie de la Paroi Arterielle (LABPART), Faculte de Medecine, 2 bis Boulevard Tonnellé, 37032 Tours, Indre et Loire, France.
Eder
Véronique
V
Rochefort
Gaël Y
GY
Hyvelin
Jean-Marc
JM
Machet
Marie Christine
MC
Fauchier
Laurent
L
Bonnet
Pierre
P
D000280:Administration, Inhalation; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002248:Carbon Monoxide / Q000633:toxicity*; D006332:Cardiomegaly / Q000503:physiopathology; D004452:Echocardiography; D006321:Heart / Q000503:physiopathology; D006333:Heart Failure / Q000473:pathology / Q000503:physiopathology; D006419:Heme Oxygenase (Decyclizing) / Q000096:biosynthesis; D006439:Hemodynamics / Q000187:drug effects; D007150:Immunohistochemistry; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology*; D010807:Physical Endurance / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D012907:Smoking / Q000473:pathology*; D020257:Ventricular Remodeling / Q000187:drug effects*
D002248:Carbon Monoxide; D006419:Heme Oxygenase (Decyclizing)