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Reactivity of pulmonary vessels to hypoxia
 Koubský, Karel ; Herget, Jan (advisor) ; Červenka, Luděk (referee) ; Neckář, Jan (referee)
Hypoxic pulmonary vasoconstriction (HPV) is a physiological mechanism that maintains optimal oxygenation of blood in the lungs. However, chronic hypoxia causes hypoxic pulmonary hypertension (HPH). Increased reactive oxygen species (ROS) participate in the pathogenesis of HPH. Oxidative stress can cause NO synthase uncoupling and subsequent production of superoxide instead of NO. Increase in intracellular Ca2+ concentration in pulmonary smooth muscle cells is required for pulmonary vasoconstriction. However, vessel tone can also be regulated by vascular smooth muscle cells' calcium sensitivity (without Ca2+ concentration changes). Increase of calcium sensitivity plays a role in HPV and HPH. This study focuses on three mechanisms to influence the increased calcium sensitivity in HPV a HPH: (1) Rho kinase inhibition, (2) effort to re-couple NO synthase, and (3) vasorelaxant effect of tyrosine kinase inhibitors. Normobaric hypoxic chamber (10% O2) or the combination of hypoxia and vascular endothelial growth factor receptor blockade was used to induce pulmonary hypertension in rats. (1) The effect of acute and chronic Rho kinase inhibition was studied on pressure-flow relationship (P/Q) in isolated perfused lungs. Acute Rho kinase inhibition decreased the basal tone of pulmonary vessels in HPH...
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