Mirza Alain, Eder Véronique, Rochefort Gaël Y, Hyvelin Jean-Marc, Machet Marie Christine, Fauchier Laurent, Bonnet Pierre
Laboratoire de Physiopathologie de la Paroi Arterielle (LABPART), Faculte de Medecine, 2 bis Boulevard Tonnellé, 37032 Tours, Indre et Loire, France.
Toxicol Sci. 2005 Jun;85(2):976-82. doi: 10.1093/toxsci/kfi139. Epub 2005 Mar 2.
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.
我们假设，吸入与烟草烟雾中浓度相似的一氧化碳（CO）（500 ppm），会通过加剧重塑过程扰乱心肌梗死后的心血管适应性。我们评估了四组大鼠。两组通过结扎左冠状动脉诱导心肌梗死：第一组暴露于空气中（梗死空气组，n = 12），第二组暴露于CO中（梗死CO组，n = 11）。将它们与两组假手术组进行比较，即对照空气组（n = 10）和暴露于CO（3周）的对照CO组（n = 7）。对梗死CO组和梗死空气组的有氧耐力能力进行了评估（耐力能力 = 0.043±0.006 m·min⁻¹·g⁻¹ 与 0.042±0.005 m·min⁻¹·g⁻¹，无显著差异）。与梗死空气组相比，梗死CO组在梗死后3周观察到左心室扩张增加（左心室舒张期（LVD）直径（D）= 9±0.4 与 7±0.4 mm，p < 0.05；左心室收缩期（LVS）直径（D）= 6±0.6 与 4.1±0.4，p < 0.05），并且舒张期后壁厚度增加（后壁舒张期厚度 = 1.7±0.1 与 1.3±0.1 mm，p < 0.05）。对两个心室和肺动脉的血流动力学压力测量显示，与空气暴露相比，CO暴露后舒张压升高（LVD压力 = 32±1.6 与 19±2.3 mmHg，p < 0.05；右心室舒张压 = 16±1.6 与 8.6±1.6 mmHg，p < 0.05；肺动脉舒张期压力（PAD）= 27±1.6 与 20±2.3 mmHg，p < 0.05）。在梗死CO组中，梗死面积增加。超声心动图和组织学显示对侧心肌壁肥厚，类似于在未梗死的对照CO组中观察到的值。总之，慢性吸入CO会通过增加梗死面积和肥厚重塑加重心肌梗死大鼠的心力衰竭。
