Study Sheds Light on Link Between Smoking, Blood Clots

Smoking associated with reduced PAR-1-related endothelial vasomotor, fibrinolytic function

TUESDAY, June 24 (HealthDay News) -- Cigarette smokers show a considerable impairment in thrombin-mediated vascular responses, with inhibition of protease-activated receptor type 1 (PAR-1)-mediated endothelial vasomotor and fibrinolytic ability, according to research published in the July 1 issue of the Journal of the American College of Cardiology.

Ninian N. Lang, of the University of Edinburgh in the United Kingdom, and colleagues analyzed data from 12 long-time smokers and 12 age- and gender-matched non-smokers. The researchers assessed subjects' forearm blood flow while administering intrabrachial infusions of the PAR-1-activating peptide SFLLRN, bradykinin and sodium nitroprusside.

The researchers report that smokers showed modest reductions in bradykinin-induced release of active tissue plasminogen activator (tPA) and reduced SFLLRN-induced vasodilatation. The smokers also had substantial impairment of SFLLRN-induced tPA antigen and activity release compared to non-smokers.

"In healthy vessels, thrombin's powerful procoagulant and prothrombotic effects are offset by its ability to evoke the release of tPA and induce arterial vasodilation. We have shown here that cigarette smoking causes a marked impairment in PAR-1-mediated endothelial vasomotor and fibrinolytic function. Relative arterial stasis and abolition of tPA release will strongly enhance clot expansion and vessel occlusion. Taken together, these findings suggest a major contribution of impaired endothelial PAR-1 action to the increased atherothrombotic risk of smokers," the authors write.

A study co-author received support from a Bristol-Myers Squibb Cardiovascular Prize Fellowship.

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