Prostacyclin production by the heart: Effect of nicotine and carbon monoxide

Effeney D.J. (1987) Prostacyclin production by the heart: Effect of nicotine and carbon monoxide. Journal of Vascular Surgery, 5 2: 237-247. doi:10.1016/0741-5214(87)90132-7


Author Effeney D.J.
Title Prostacyclin production by the heart: Effect of nicotine and carbon monoxide
Journal name Journal of Vascular Surgery   Check publisher's open access policy
ISSN 0741-5214
Publication date 1987-01-01
Sub-type Article (original research)
DOI 10.1016/0741-5214(87)90132-7
Open Access Status Not yet assessed
Volume 5
Issue 2
Start page 237
End page 247
Total pages 11
Subject 2705 Cardiology and Cardiovascular Medicine
2746 Surgery
Abstract Smoking has been linked to the development and progression of atherosclerosis but the mechanism by which smoking exerts its deleterious effects remains unknown. This study was designed to examine in a systematic way the effects of nicotine and carbon monoxide on platelets, arterial walls, and the heart. Results of experiments designed to assess the effect of nicotine and carbon monoxide on the production of prostacyclin (PGI2) by the rabbit heart are reported. Animals exposed to carbon monoxide had the carboxyhemoglobin raised to at least 12% by breathing an atmosphere enriched with carbon monoxide. Nicotine was infused at 50 μg/kg/hr for 1 week. Nicotine was measured by gas/liquid chromatography. PGI2 was measured by radioimmunoassay of 6-keto-PGF1α, and its biologic activity was assessed by inhibition of platelet aggregation. Nicotine is concentrated in the heart and blood vessel wall and causes a statistically significant reduction in PGI2 production. Carbon monoxide raised PGI2 production significantly in all chambers, and the combination of nicotine and carbon monoxide further raised PGI2 production. The difference between the effects of nitrogen and carbon monoxide alone and nitrogen and a combination of nitrogen and carbon monoxide was significant in all chambers. It is hypothesized that nicotine exerts a direct metabolic effect in lowering PGI2 production. Carbon monoxide may make the endothelial cell relatively hypoxic, a powerful stimulus of PGI2 production, or less likely exert a direct toxic effect on the endothelial cell.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: Scopus Import - Archived
 
Versions
Version Filter Type
Citation counts: Scopus Citation Count Cited 11 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Tue, 28 Jun 2016, 15:08:58 EST by System User