engleski

yperbaric oxygenation and modulation of membrane ion channels important in the mechanisms of vasorelaxation and vasoconstriction

Oxygen is a highly reactive molecule which, at high partial pressures (like in HBO2), can contribute to the increased formation of ROS and affect system hemodynamics and vascular function. Our studies showed that acute exposure to HBO2 increased plasma oxidative stress (measured by lipid peroxidation products), increased pO2 in healthy SD rats and decreased pH and pCO2 in arterial blood and impaired vascular relaxation to acetylcholine and hypoxia. On the other hand, intermittent HBO2 restored vascular relaxation, and changed the metabolic pathways involved in the vasorelaxation in healthy and diabetic animals (1-6). Enzymes that appear to function as cellular pO2sensors include oxygenase enzymes generating mediatorssuch as eicosanoids and nitric oxide that regulate signaling processes and vasomotion (vasodilation and vasoconstriction).Intracellular processes in vascular smooth muscle thatseem to be regulated by acute changes in pO2 include K+channels, systems controlling intracellular Ca2+ , and the activity of sGC. Vasodilation is also affected by EDHFs like potassiumions, hydrogen peroxide (H2O2) and EETs (7-11). It is believed that some of them may cause hyperpolarization through the myo-endothelial tight connectors. Vasodilation occurs when a specific stimulation of the endothelial cell causes hyperpolarization of the smooth muscle cell by opening large conductive calcium activated potassium channels, hyperpolarization then inhibits calcium channels and thus prevents calcium ions from entering the smooth muscle cell resulting in vasodilation (8). Taken together, HBO2 may influence functional and structural characteristics of blood vessels and modulate membrane ion channels involved in vasodilation, depending on the application protocol.

hyperbaric oxygenation ; membrane ion channels ; vasorelaxation ; vasoconstriction

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