In view of the perplexities in attributing the real cause of the cardiovascular changes that may occur in carbon monoxide (CO) intoxication to the known pathogenetic mechanism, a study was made on 52 volunteers who were submitted to inhalation of a mixture containing CO (an almost three-fold increase of HbCO over basal values), in order to measure possible changes in platelet aggregation. Thromboxane B2 (TxB2), beta thromboglobuline in urine (βTGU) and 6 oxoprostaglandin f1alpha (6-K-PGF). A statistically significant increase in platelet aggregation was observed after CO inhalation and TxB2 and βTGU were also markedly elevated; 6-K-PGF1 however was not appreciably modified. The changes were found to be specific for CO exposure since they were not observed in another group of 28 volunteers submitted under the same conditions to breathing a hypoxic mixture causing a similar O2 desaturation. The comparison between the two groups was statistically significant for CO exposure. These findings are discussed in relation to the type of hemorheologic and histologic changes induced by aggregated platelets and hyperaggregation consequent to CO exposure might be the real pathogenetic mechanism responsible for the onset or aggravation of cardiovascular modification in CO intoxication. This interpretation could lead to the establishement of better preventive measures for exposed workers and more appropriate treatment of CO intoxication.
|Number of pages||8|
|Journal||Medicina del Lavoro|
|Publication status||Published - 1988|
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health