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

Artery. 1982;10(6):412-9.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenosine Diphosphate / pharmacology
  • Animals
  • Aorta / metabolism*
  • Carbon Monoxide / pharmacology*
  • Epoprostenol / biosynthesis*
  • Male
  • Nicotine / pharmacology*
  • Platelet Aggregation / drug effects
  • Prostaglandins / biosynthesis*
  • Rats

Substances

  • Prostaglandins
  • Adenosine Diphosphate
  • Nicotine
  • Carbon Monoxide
  • Epoprostenol