Favory Raphaël, Lancel Steve, Tissier Stéphanie, Mathieu Daniel, Decoster Brigitte, Nevière Rémi
Intensive Care Unit and Hyperbaric Regional Center, University Hospital of Lille, Lille, France.
Am J Respir Crit Care Med. 2006 Aug 1;174(3):320-5. doi: 10.1164/rccm.200601-117OC. Epub 2006 May 11.
Results from both animal and human being studies provide evidence that inhalation of concentrations of carbon monoxide (CO) at around 100 ppm has antiinflammatory effects. These low levels of CO are incriminated in ischemic heart diseases experienced by cigarette smokers and, in some cases, from air pollution. Although neurologic mechanisms have been investigated, the effects of CO on cardiovascular function are still poorly understood.
The effects of CO (250 ppm; 90 min) inhalation on myocardial function were investigated in isolated heart of rats killed immediately, and 3, 24, 48, and 96 h after CO exposure. CO exposure at 250 ppm resulted in an arterial carboxyhemoglobin (HbCO) level of approximately 11%, 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 -independent vascular relaxation abnormalities. CO-induced coronary vascular relaxation perturbations were observed in the presence of increased heart contractility. Spontaneous peak to maximal Ca(2+)-activated left ventricular pressure ratio was markedly increased in CO-exposed rats, indicating increases in myofilament calcium sensitivity. Heart cyclic guanosine monophosphate/cAMP ratio and myocardial permeabilized fiber respiration (complex intravenous activity) were reduced in CO-exposed rats, which lasted after 48 h of reoxygenation in air.
These findings suggest that CO deteriorates heart oxygen supply to utilization and potentially may induce myocardial hypoxia through mechanisms that include increased oxygen demand due to increased contractility, reduced coronary blood flow reserve, and cardiomyocyte respiration inhibition.
动物和人体研究结果均表明，吸入浓度约为100 ppm的一氧化碳（CO）具有抗炎作用。这些低水平的CO与吸烟者患缺血性心脏病以及某些情况下与空气污染导致的缺血性心脏病有关。尽管已经对神经机制进行了研究，但CO对心血管功能的影响仍知之甚少。
研究了吸入CO（250 ppm；90分钟）对立即处死的大鼠离体心脏以及CO暴露后3、24、48和96小时的大鼠离体心脏心肌功能的影响。暴露于250 ppm的CO导致动脉血中碳氧血红蛋白（HbCO）水平约为11%，这与平均动脉压和心率的变化无关。CO暴露导致冠状动脉灌注压升高，这与内皮依赖性和非依赖性血管舒张异常有关。在心脏收缩力增加的情况下，观察到CO诱导的冠状动脉血管舒张紊乱。暴露于CO的大鼠中，自发峰值与最大Ca(2+)激活的左心室压力比显著增加，表明肌丝钙敏感性增加。暴露于CO的大鼠心脏环磷酸鸟苷/环磷酸腺苷比值和心肌通透纤维呼吸（复合静脉活性）降低，在空气中复氧48小时后仍持续存在。
这些发现表明，CO会恶化心脏的氧供应与利用，并且可能通过包括因收缩力增加导致氧需求增加、冠状动脉血流储备减少以及心肌细胞呼吸抑制等机制诱导心肌缺氧。
