Chronic exposure to cigarette smoke causes an imbalance in the ratio of PGI2 and TXA2 production and is believed to favor the development of atherosclerosis. Components of the particulate phase of smoke (especially nicotine) as well as the gas phase of smoke have been shown to adversely alter arachidonic acid metabolism. To determine the relative participation of nicotine, particulate and gas phases in eliciting an imbalance in TXA2 formation, male Sprague-Dawley rats were chronically exposed (7 days/wk/mo.) to freshly generated whole smoke or gas phase from University of Kentucky Reference cigarettes and allowed access to regular drinking water or to water supplemented with nicotine (10 μg/ml). COHb levels were monitored to confirm smoke or gas phase inhalation. All treatment groups had lower body weights than shams. No differences in body weights were observed between smoke (± oral nicotine) and gas phase (± oral nicotine) treatment groups but all were significantly lower than oral nicotine treated animals. Platelet TXA2 production was elevated in all treatment groups compared to shams. No differences in TXA2 production were observed between smoke (± oral nicotine), gas phase and oral nicotine treated animals. Animals receiving gas phase/oral nicotine exhibited significantly higher platelet TXA2 production compared to the other treatments. Constituents of the gas phase as well as the particulate phase of whole smoke were both shown to elevate platelet TXA2 formation. Compenent(s) of the particulate matter appear to modulate the effects of nicotine and the gas phase in the perturbation of TXA2 production in the rat smoking model.
|Number of pages||4|
|Journal||Prostaglandins, Leukotrienes and Essential Fatty Acids|
|State||Published - 1 Jan 1988|