Intravascular release of a platelet-activating factor-like lipid (PAF-LL) induced by cigarette smoking.

To assess the role of platelet-activating factor (PAF) in smoking-induced vascular injury, the effect of cigarette smoking on PAF-like lipid (PAF-LL) in plasma was studied. The subjects were 12 young smokers (22 +/- 1.3 years old), 13 young non-smokers (22 +/- 2.1 years old), 14 older smokers (59 +/- 9.6 years old), and 11 older nonsmokers (60 +/- 8.7 years old). Lipids were extracted from 5 mL of plasma and then were separated by thin-layer chromatography. The fraction with the same migration as authentic PAF was recovered and tested for the ability to aggregate human polymorphonuclear neutrophils (PMN). The activity was identified as PAF-LL because it was inactivated by phospholipase A2, and because the effects on PMN were blocked by CV-3988, a competitive antagonist of the PAF receptor. PAF-LL was detected in plasma from 3 young non-smokers (23%), 5 young smokers (42%), 3 older non-smokers (27%) and 11 older smokers (79%). The incidence of the detection of plasma PAF-LL in older smokers was significantly higher than those in young non-smokers (p less than 0.01) or in older non-smokers (p less than 0.05). In young smokers, the acute effect of smoking was also studied. Plasma PAF-LL was detected in all of the 12 subjects immediately after smoking a cigarette, in sharp contrast to the incidence of 42% before smoking. Plasma beta-thromboglobulin was highest in older smokers, and it increased significantly after smoking a cigarette in young smokers. Smoking is associated with increased production of PAF or a similar lipid, which may play an important role in the pathogenesis of smoking-induced vascular diseases.