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Short repeated cycles of peripheral ischemia/reperfusion (I/R) can protect distant organs from subsequent prolonged I/R injury; a phenomenon known as remote ischemic preconditioning (RIPC). A RIPC-mediated release of humoral factors might play a key role in this protection and vascular endothelial cells are potential targets for these secreted factors. In the present study, RIPC-plasma obtained from healthy male volunteers was tested for its ability to protect human umbilical endothelial cells (HUVEC) from hypoxia–induced cell damage. 10 healthy male volunteers were subjected to a RIPC-protocol consisting of 4 × 5 min inflation/deflation of a blood pressure cuff located at the upper arm. Plasma was collected before ( T 0; control), directly after ( T 1) and 1 h after ( T 2) the RIPC procedure. HUVEC were subjected to 24 h hypoxia damage and simultaneously incubated with 5 % of the respective RIPC-plasma. Cell damage was evaluated by lactate dehydrogenase (LDH)-measurements. Western blot experiments of hypoxia inducible factor 1 alpha (HIF1alpha), phosphorylated signal transducer and activator of transcription 5 (STAT5), protein kinase B (AKT) and extracellular signal-related kinase 1/2 (ERK-1/2) were performed. Furthermore, the concentrations of hVEGF were evaluated in the RIPC-plasma by sandwich ELISA. Hypoxia–induced cell damage was significantly reduced by plasma  T 1 ( p  = 0.02 vs  T 0). The protective effect of plasma  T 1 was accompanied by an augmentation of the intracellular HIF1alpha ( p  = 0.01 vs  T 0) and increased phosphorylation of ERK-1/2 ( p  = 0.03 vs  T 0). Phosphorylation of AKT and STAT5 remained unchanged. Analysis of the protective RIPC-plasma  T 1 showed significantly reduced levels of hVEGF ( p  = 0.01 vs  T 0). RIPC plasma protects endothelial cells from hypoxia–induced cell damage and humoral mediators as well as intracellular HIF1alpha may be involved.

Plasma from human volunteers subjected to remote ischemic preconditioning protects human endothelial cells from hypoxia–induced cell damage