Becker L C, Haak E D
Arch Environ Health. 1979 Jul-Aug;34(4):274-9. doi: 10.1080/00039896.1979.10667413.
This study was conducted to determine whether low level exposure to carbon monoxide would increase myocardial ischemia associated with acute myocardial infarction. An hour after coronary artery ligation, eleven anesthetized dogs underwent five sequential respiratory exposures to 5,000 ppm carbon monoxide, producing mean blood carboxyhemoglobin levels of 4.9% to 17.0%. Ischemia, as indicated by the amount of S-T segment elevation in epicardial electrocardiograms, increased significantly at the lowest carboxyhemoglobin level and increased further with increasing carbon monoxide exposure. These changes occurred in the absence of altered heart rate, blood pressure, left atrial pressure, cardiac output, or blood flow to ischemic myocardium. Flow to non-ischemic myocardium increased with carbon monoxide exposure, the percentage increase being approximately double the increase in carboxyhemoglobin level. Thus, low level exposure to carbon monoxide can significantly augment ischemia in acute myocardial infarction, apparently through a reduction in oxygen supplied to ischemic tissue. The data suggest that hypoxia induced by carbon monoxide exposure is more severe than can be accounted for by a simple reduction in oxygenated hemoglobin.
本研究旨在确定低水平接触一氧化碳是否会增加与急性心肌梗死相关的心肌缺血。冠状动脉结扎一小时后,11只麻醉犬依次进行5次呼吸暴露于5000 ppm一氧化碳的实验,使血液中碳氧血红蛋白平均水平达到4.9%至17.0%。根据心外膜心电图中S-T段抬高的程度所示,缺血在最低碳氧血红蛋白水平时显著增加,并随着一氧化碳暴露增加而进一步加重。这些变化发生时,心率、血压、左心房压力、心输出量或缺血心肌的血流量均未改变。一氧化碳暴露后,非缺血心肌的血流量增加,增加的百分比约为碳氧血红蛋白水平增加的两倍。因此,低水平接触一氧化碳可显著加重急性心肌梗死时的缺血,显然是通过减少供应给缺血组织的氧气实现的。数据表明,一氧化碳暴露引起的缺氧比单纯因氧合血红蛋白减少所能解释的更为严重。