Smoking alters thromboxane metabolism in man

Abstract

Chronic smoking is a major risk factor of atherosclerosis and coronary heart disease. The measurement of three major thromboxane A 2 metabolites, 11-dehydrothromboxane B 2, 2,3-dinorthromboxane B 2 and thromboxane B 2, in the urines of 13 apparently healthy smokers (average 39 years, range 27–56 years) showed significantly elevated excretion rates for all thromboxane A 2 metabolites as compared to 10 apparently healthy age-matched non-smokers (average 37 years, range 26–56 years). Importantly, characteristic alterations in the thromboxane A 2 metabolite pattern were found in the urines of smokers. The contribution of 2,3-dinorthromboxane B 2 to total measured excretion of thromboxane A 2 metabolites was 59.2% in smokers (404.0 ± 53.0 pg/mg creatinine) versus 19.4% in non-smokers (85.2 ± 8.3 pg/mg creatinine), that of 11-dehydrothromboxane B 2 35.7% in smokers (673.2 ± 88.9 pg/mg creatinine) as compared to 75.5% in non-smokers (332.6 ± 30.9 pg/mg creatinine). The contribution of thromboxane B 2 (57.5 ± 7.7 pg/mg creatinine in smokers versus 21.9 ± 1.5 pg/mg creatinine in non-smokers) was similar at 5.1%. The excretion of cotinine, the major urinary metabolite of nicotine that correlates well with the reported daily cigarette consumption ( r = 0.97, P < 0.0001), showed a good correlation to thromboxane A 2 metabolite excretion (2,3-dinorthromboxane B 2: r = 0.92, P < 0.0001; 11-dehydrothromboxane B 2; r = 0.87, P < 0.0001).