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 dete...

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Bibliographic Details
Published in:	Artery Vol. 10; no. 6; p. 412
Main Authors:	Hartiala, J, Simberg, N, Uotila, P
Format:	Journal Article
Language:	English
Published:	United States 1982
Subjects:	Adenosine Diphosphate - pharmacology Animals Aorta - metabolism Carbon Monoxide - pharmacology Epoprostenol - biosynthesis Male Nicotine - pharmacology Platelet Aggregation - drug effects Prostaglandins - biosynthesis Rats
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Summary:	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.
ISSN:	0098-6127