Sixteen rabbits were placed in exposure chambers: eight were continuously exposed to 180 ppm of carbon monoxide and eight were exposed to atmospheric air for 2 weeks. The myocardial ultrastructure of all the rabbits was examined. In rabbits exposed to carbon monoxide, local areas of partial or total necrosis of the myofibrils and degenerative changes of the mitochondria were found. Extra- and intracellular edema, increases in the number of ribosomes and lipofuscin granules, and reparative fibrotic changes also occurred. Varying degrees of injury were noted in the blood vessels. Capillary edema, but never total stenosis, was seen in some areas. Stasis and occasional small perivascular hemorrhages were typical on the venous side; on the arterial side the characteristic picture was one of endothelial swelling, formation of subendothelial edema, and degenerative changes of the myocytes. The present study supports the hypothesis that chronic exposure to low levels of carboxyhemoglobin can produce myocardial damage and account for the increased risk of myocardial infarction and sudden death seen in heavy cigarette smokers.
Kjeldsen et al. (Fri,) studied this question.