Surfaces of apoptotic and necrotic blood cells allow initiation of coagulation cascade by tissue factor derived from monocytes. Openers of KATP-channels were shown to prevent apoptosis in several cell types. The aim of the present study was to characterize molecular subunits of KATP-channels in human monocytes and to study the effect of KATP-modulators on apoptosis/necrosis induced by blood stasis.

Stasis was simulated ex vivo, also in presence of 30 mM pinacidil (KATP-opener) or 30 mM glibenclamide (KATP-blocker). Early apoptotic cells were stained with AnnexinV-FITC and Anti CD14-PerCP antibodies after 2 and 8h of stasis.

Results: mRNAs of the KATP-channel subunits KIR6.1 and Kir6.2 could be detected in CD14+ cells. However neither SUR1-nor SUR2a/SUR2b subunit-mRNAs could be found.

In the course of simulated ex vivo stasis, the fraction of apoptotic/necrotic CD14+ cells increased from 0.7% after 2h to 4.1% after 8h. In presence of pinacidil less cells died (1% and 0.9%, after 2 and 8h, resp.). In contrast, in presence of glibenclamide this fraction increased from 2.1% (2h) to 8,8% (8h). Conclusion: Human monocytes express both Kir6.1 and Kir6.2 isoforms and opening of these channels by pinacidil prevents