Objective:
For patients undergoing surgery, quitting smoking prior to surgery is recommended, since smoking increases the risk of postoperative morbidity or mortality. Although smoking is recognized to change the hemostatic process, the influences of smoking and smoking cessation on human platelet activation remain controversial. Since collagen initiates human platelet activation in the process of thrombus formation, we investigated the effects of smoking cessation on human platelet activation induced by collagen.

Methods:
We enrolled patients in smoking cessation outpatient services (n=19). Blood samples were donated before smoking cessation, 4, 8 and 12 weeks after smoking cessation. We investigated the size of platelet aggregation using laser scattering methods. We examined the effects of collagen on platelet aggregation, the secretion of platelet-derived growth factor (PDGF)-AB and the levels of collagen-induced phosphorylation of p38 mitogen-activated protein (MAP) kinase.

Results:
A low dose of collagen (1 µg/ml) accelerated platelet aggregation at 4 or 8 weeks after smoking cessation compared with before cessation. After 12 weeks, the levels of platelet aggregation induced by collagen were almost to the levels before smoking cessation. The collagen-induced PDGF-AB secretion levels at 4 or 8 weeks after quitting smoking were significantly higher than before quitting smoking. Smoking cessation strengthened the collagen-induced phosphorylation of p38 MAP kinase after 4 weeks.

Conclusions:
Our results strongly suggest that smoking cessation causes temporary hyper-activation of human platelets in the short term. We may be able to reduce the incidence of complications due to hyper-reactivity of human platelets by considering the smoking abstinence period.