Alterations in prostacyclin and thromboxane formation following chronic exposure to high and low nicotine cigarettes in rats.
Chronic exposure to cigarette smoke causes an imbalance in both PGI2 and TXA2 production which is believed to favor the development of atherosclerosis. Nicotine, a major constituent of smoke, has been shown to adversely alter arachidonic acid metabolism. To determine whether varying doses of nicotine in cigarettes would influence the extent of PGI2/TXA2 alterations, male Sprague-Dawley rats were chronically exposed (7 days/wk/6 mo.) to smoke from University of Kentucky Reference cigarettes containing "low" nicotine (3A1), "high" nicotine (2R1) and "low" nicotine cigarettes spiked with enough nicotine to deliver amounts equivalent to the 2R1. COHb levels were monitored to confirm smoke inhalation. No differences in body weights were observed between treatment groups, but all were significantly lower than sham. Aortic PGI2 formation was not significantly depressed by any of the treatment groups compared to shams. Platelet TXA2 production was elevated in all treatment groups compared to shams, irrespective of nicotine content. In the rat smoking model, low nicotine cigarettes do not appear to be an advantage over higher nicotine cigarettes.
Sherratt
A J
AJ
Culpepper
B T
BT
Lubawy
W C
WC
D000818:Animals; D001011:Aorta / Q000378:metabolism; D002263:Carboxyhemoglobin / Q000378:metabolism; D011464:Epoprostenol / Q000096:biosynthesis*; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D010947:Plants, Toxic; D051381:Rats; D011919:Rats, Inbred Strains; D012906:Smoke / Q000009:adverse effects*; D013928:Thromboxane A2 / Q000096:biosynthesis*; D013997:Time Factors; D014026:Nicotiana
D012906:Smoke; D013928:Thromboxane A2; D009538:Nicotine; D002263:Carboxyhemoglobin; D011464:Epoprostenol