• 1 January 1982
    • journal article
    • research article
    • Vol. 10  (6) , 412-419
Abstract
The effects of nicotine and CO on the production of PGI2 by rat arterial rings were studied. For PGI2 analysis, a bioassay based on platelet-rich plasma aggregation with ADP was used. Neither nicotine in the incubate nor pretreatment with CO decreased PGI2 production as detectable in this bioassay system. Neither had a direct effect on the ADP-induced aggregability of human platelet-rich plasma. Consequently, these agents do not seem to be responsible for the temporary increase in platelet aggregability after cigarette smoking. [The involvement of smoking in atherosclerosis is discussed].