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.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000378:metabolism*; D002248:Carbon Monoxide / Q000494:pharmacology*; D011464:Epoprostenol / Q000096:biosynthesis*; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats
D011453:Prostaglandins; D000244:Adenosine Diphosphate; D009538:Nicotine; D002248:Carbon Monoxide; D011464:Epoprostenol