Exposure to carbon monoxide or to nicotine does not inhibit PGI2 formation by rat arterial rings incubated with human platelet-rich plasma.

The effects of nicotine and carbon monoxide on the production of PGI2 by rat arterial rings were studied. For PGI2 analysis, we used a bioassay based on platelet-rich plasma aggregation with ADP. Neither nicotine in the incubate nor pretreatment with carbon monoxide decreased PGI2-production as detectable in this bioassay system. Also, 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.