treating disorders other than decompression sickness. Still, HBO2is a treatmentmodality that has gained recognition in certain situations of ischaemia reper fusion. However, not much is known about its eVect on the endothelial cells.Based on earlier studies, the hypothesis was that HBO2treatment stimulates therelease of brinolytic factors. The aim of the study was to investigate the eVectof HBO2treatment on cultured endothelial cells in a simulated ischaemia reperfusion model. Methods: To mimic the clinical situation during ischaemiareperfusion, endothelial cells were subjected to anoxia for 8 h, followed by reper fusion with either HBO2 or normobaric air for 1.5 h, and compared with anuntreated control that was not exposed to anoxia. Components investigated werethe brinolytic stimulatortissue plasminogen activator(t-PA), urokinaseplasmin ogen activator (uPA) and the antagonist, plasminogen activator inhibitor type one (PAI-1). Results: Immediately after 8 h of total anoxia and reoxygenationwith HBO2(for 1.5 h), the mean (SEM) concentrations of t-PA, PAI-1 and uPAwere signi cantly increased compared to the other groups. The diVerence betweenthe normobaric and control groups, measured at 1.5 h, 6 h and 24 h post-anoxia,persisted throughout the experiment. Conclusion: In this ischaemia-reperfusionmodel, HBO2 stimulates the release of brinolytic factors. These observationsmight be relevant in trauma care in preventing thromboses and/or microemboliz ation following ischaemia-reperfusion.
Categories: Dermatology, Medical clinic, Rheumatology