The Effects of Chronic Smoking on the Fibrinolytic Potential of Plasma and Platelets

Abstract

Summary.We studied tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) in healthy individuals divided by smoking habit into current smokers, former smokers and non-smokers (who had never smoked). Plasma PAI-1 antigen was significantly higher in smokers than in non-smokers with intermediate levels in former smokers. A similar trend was observed for plasma PAI activity but this did not reach 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 change in plasma PAI-1 was observed. The ratio of t-PA to PAI-1 in plasma was similar in non-smokers and former smokers but lower in smokers, suggesting that there is at least partial restoration of plasma fibrinolytic potential after smoking cessation. Plasma PAI-1 antigen and PAI activity correlated with estimated pack-years of cigarettes smoked among smokers and former smokers. When all subjects were studied collectively, plasma PAI-1 correlated strongly with plasma t-PA and triglycerides; plasma t-PA also correlated strongly with triglycerdes.We conclude that chronic smoking is associated with impaired fibrinolysis in plasma and that this largely reflects elevated plasma PAI-1 in smokers. Smoking 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. Stopping smoking appears to return impaired fibrinolysis towards normal. Smoking does not quantitatively affect the platelet pool of PAI-1. Smoking habit should be controlled for in clinical analyses of PAI-1 and t-PA.

Plasminogen-activator-inhibitor-1 promoter polymorphism as a risk factor for adult periodontitis in non-smokers

“…10,17 Also chronic smoking has been associated with impaired fibrinolysis in plasma and this largely reflected elevated plasma PAI-1 in smokers. 14 It is interesting that the genetic association of the functional promoter polymorphism in the PAI-1 gene with periodontitis in our study was observed only in the group of non-smokers. The impairment of the fibrinolytic mechanisms in smokers may occur as a consequence of smoking which is known to increase the levels of PAI-1, thus possibly masking the influence of individual variants of the PAI-1 polymorphism.…”

“…10 PAI-1 than those with one or two copies of the 5G allele; 10 the 5G allele is characterized by a lower transcriptional rate of the PAI-1 gene because of binding a transcriptional repressor protein which cannot be bound by the 4G allele. 10,12 Since the 4G allele of the 4G/5G promoter polymorphism of the PAI-1 gene and/or smoking have been previously associated with increased plasma levels and activity of PAI, 13,14 we investigated the role of this polymorphism in the pathogenesis of adult periodontitis with regard to smoking status.…”

Smoking and Aortic Diseases

“…1 Smoking acts synergistically with other vascular risk factors (eg, hypertension, dyslipidaemia and diabetes) to increase vascular morbidity and mortality. 2 However, smoking has a variable magnitude of increased risk for different vascular diseases: the risk is highest for peripheral arterial disease and aortic aneurysm, and is lowest for coronary artery and cerebrovascular diseases.…”

A Ten Year Overview of Surgical and Interventional Arrhythmology in Russia. Service Peculiar Features in the Far East

“…Результаты, полученные в много-численных наблюдательных когортных, эксперименталь-ных и лабораторных исследованиях на людях и животных [225,[227][228][229], выявили механизмы влияния курения на эндотелиальную функцию [230,231], окислительные процессы [232], функцию тромбоцитов [233], фибринолиз, воспаление [234][235][236][237][238], вазомоторную функцию и модифи-кацию липидов . Активные формы кислорода -свободные радикалы -находящиеся во вдыхаемом дыму являются причиной окисления ЛПНП в плазме крови; окисленные ЛПНП, стимулируют процессы воспаления за счет прили-пания моноцитов к стенке сосудов, что является пусковым механизмом воспалительных изменений в интиме артерий, который приводит к прогрессированию атеросклероза [232,[239][240][241][242] .…”