Hyperbaric oxygen. Effects on ischemia-reperfusion

• Treatment with hyperbaric oxygen (HBO2) is controversial when treating other disorders than decompression sickness. However, HBO2 is a treatment modality that has gained recognition in certain ischemia-reperfusion situations. The aim of the present investigation was to test the hypothesis that, following trauma and ischemia-reperfusion HBO2 inhibits the activation of leukocytes and affects endothelial fibrinolysis.The effects of HBO2 on leukosequestration, measured by a ?-counter calculating leukocyte transit factor and on extracellular superoxide production, measured by nitroblue tetrazolium reduction test (NBT), were studied in two animal models; in the first instance using rats subjected to intestinal ischemia followed by reperfusion and in the second using rats with activation of the leukocytes through activation of the complement system. The effect of hyperbaric oxygen on human leukocytes in vitro, activated with phorbol myristate acetate (PMA) and f-Met-Leu-Phe (f-MLP), was studied, measuring extracellular superoxide production with NBT-test, cytochrome C reduction test and chemiluminescence.The effect of HBO2 on endothelial fibrinolysis analysis of the expression of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor type 1 (PAI-1) and urokinase plasminogen activator (uPA) with ELISA and PCR technique was studied in two in vitro models.Hyperbaric oxygen reduced the pulmonary leukosequestration following ischemia-reperfusion and inhibited the extracellular production of superoxide in activated neutrophils compared to controls. This effect is on a cellular level. Hyperbaric oxygen affected the fibrinolysis by an elevated secretion of t-PA, PAI-1 and uPA.In conclusion: Neutrophil activation following ischemia-reperfusion and complement activation was inhibited by HBO2 in vivo. Pulmonary leukosequestration following ischemia-reperfusion was inhibited by HBO2 in vivo. Normobaric and hyperbaric oxygen treatment in vitro inhibit neutrophil respiratory burst, following activation by PMA and f-MLP. Hyperbaric oxygen stimulated the endothelial fibrinolytic system.Thus, hyperbaric oxygen treatment could be beneficial in clinical states of trauma and ischemia-reperfusion.

Nyckelord

fibrinolysis

f-MLP

human

hyperbaric oxygen

neutrophils

normobaric

PAI-1

PMA

rat

t-PA

trauma

uPA

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