THE EFFECTS OF CHRONIC SMOKING ON THE FIBRINOLYTIC POTENTIAL OF PLASMA AND PLATELETS

We studied tissue-type plasminogen activator (t-PA) and plasminogen ac tivator inhibitor typ 1 (PAI-1) in healthy individuals divided by smok ing habit into current smokers, former smokers and non-smokers (who ha d never smoked). Plasma PAI-1 antigen was significantly higher in smok ers than in non-smelters with intermediate levels in former smokers. A similar trend was observed for plasma PAI activity but this did not r each statistical significance. Platelet PAI-1 and plasma t-PA were not significantly different when comparing the three groups. After venous occlusion t-PA rose significantly in all groups; no significant chang e in plasma PAI-1 was observed. The ratio of t-PA to PAI-1 in plasma w as similar in non-smokers and former smokers but lower in smelters, su ggesting that there is at least partial restoration of plasma fibrinol ytic potential after smoking cessation. Plasma PAI-1 antigen and PAI a ctivity correlated with estimated pack-years of cigarettes smoked amon g smokers and former smokers. When all subjects were studied collectiv ely plasma PAI-1 correlated strongly with plasma t-PA and triglyceride s; plasma t-PA also correlated strongly with triglycerdes. We conclude that chronic smoking is associated with impaired fibrinolysis in plas ma and that this largely reflects elevated plasma PAI-1 in smelters. S moking does not appear to affect the response to venous occlusion. The postulated effect of chronic smoking on plasma PAI-1 may be mediated by the influence of smoking on triglycerides and insulin resistance. S topping smoking appears to return impaired fibrinolysis towards normal . Smoking does not quantitatively affect the platelet pool of PAI-I. S moking habit should be controlled for in clinical analyses of PAI-1 an d t-PA.