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Implication des canaux potassiques dans l'hyporéactivité vasculaire observée au cours des états de choc

Abstract : Several mechanisms have been proposed to explain the pathophysiology of vascular failure induced by shock states, including those involving nitric oxide (NO) and potassium channels. In this experimental study, we hypothesized that during shock state, in addition to their activation, the expression of vascular potassium channels is increased regardless of the etiology of shock, and that this increase is at least partially linked to NO over-production. Our results demonstrate that ATP-dependent potassium channels (KATP), unlike the calcium-dependent potassium channels (BKCa) play a crucial role in vascular adaptation to hemorrhagic and septic shock, due to restoration of vasoreactivity by using PNU-37883A, a pore-specific inhibitor of KATP channels, and not by using iberiotoxin, a specific inhibitor of BKCa channels. We also demonstrate that the expression of vascular KATP channels is increased in experimental hemorrhagic and septic shock. Furthermore, we demonstrate in vivo that the up-regulation of vascular KATP channels is partially related to increase in expression of inducible NO synthase (iNOS), probably via nuclear factor-kappa B (NK-kB) activation and is responsible for the reduction of vascular tone
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  • HAL Id : tel-01746262, version 1



Solène Collin. Implication des canaux potassiques dans l'hyporéactivité vasculaire observée au cours des états de choc. Médecine humaine et pathologie. Université Henri Poincaré - Nancy 1, 2011. Français. ⟨NNT : 2011NAN10104⟩. ⟨tel-01746262⟩



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