Local hypoxemia occurring in insufficiently flowing blood is an important factor for the development of stasis-induced venous thrombosis, which can potentially cause terminal embolism. The mechanisms by which hypoxemia triggers thrombosis are still incompletely understood. Monocytes are known to adopt procoagulatory properties, upregulation and de-encryption of tissue factor upon activation (Luther et al. 1990; Lawson et al. 1997). Since metabolism sensitive KATP-channels were identified previously on bovine monocytes (Loehrke et al. 1997), the aim of the present study was to investigate the role of KATP-channels on human monocytes for initiating a procoagulatory state under stasis conditions. Stasis was simulated ex vivo by incubating whole blood of healthy men (n=3) at 37°C in tightly sealed tubes and slight mechanical agitation, while pO2 was deliberately allowed to deplete (pO2 depletion rate: 7% per hour). Tissue Factor Coagulation Time (Santucci et al. 2000) (TiFaCT) in whole blood was measured in quadruples after 2 and 6 h of stasis, in presence of 100 uM KATP-channel blocker glibenclamide or 30 uM KATP-channel opener pinacidil and each of these in presence of 10 ug/ml LPS. TF-expression on CD14- positive monocytes was quantified by flow cytometry (AntiCD142-PE, clone HTF-1, AntiCD14-PerCP, clone mPhiP89). With increasing time stasis (control) leads to acceleration of TiFaCT (93.43 ± 2.4 and 76.97 ± 1.28 sec after 2 or 6 h, resp.). LPS further stimulated clotting (88.49 ± 3.23 and 64.42 ± 0.66, resp.) In the presence of pinacidil this phenomenon is even further enhanced (83.57 ± 1.92 and 56.3 ± 1.01 sec, resp.). Also pinacidil alone leads to a slightly accelerated clotting (aprox. 10%) after 6 h of stasis compared to control. Glibenclamide inhibits LPS-induced accelerated clotting by 10% after 2h. Glibenclamide alone decelerates clotting by 3% after 6h of stasis. Flow cytometry shows 1.64 and 2.8% TF positive CD14+ cells after 2 and 8 h of stasis, resp. Pinacidil enhances TF expression in 2.65 and 12.2% of cells, resp. In presence of glibenclamide, 1.55 and 2.3%, resp., of CD14+ cells were TF-positive. As a preliminary conclusion, KATP-channels seem to be involved in the acceleration of blood clotting under stasis conditions and clearly modulate coagulation in the case of strong concomitant LPS-stimulation. Further studies are necessary to identify molecular identity of the monocytic KATP-channels and to clarify the signalling pathway involved.