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- aggregation classification "A1".
- aggregation creator B419599.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation date "2010".
- aggregation format "application/pdf".
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- aggregation isPartOf urn:issn:0946-2716.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Reactive oxygen species and small-conductance calcium-dependent potassium channels are key mediators of inflammation-induced hypotension and shock".
- aggregation abstract "Septic shock is associated with life-threatening vasodilation and hypotension. To cause vasodilation, vascular endothelium may release nitric oxide (NO), prostacyclin (PGI2), and the elusive endothelium-derived hyperpolarizing factor (EDHF). Although NO is critical in controlling vascular tone, inhibiting NO in septic shock does not improve outcome, on the contrary, precipitating the search for alternative therapeutic targets. Using a hyperacute tumor necrosis factor (TNF)-induced shock model in mice, we found that shock can develop independently of the known vasodilators NO, cGMP, PGI2, or epoxyeicosatrienoic acids. However, the antioxidant tempol efficiently prevented hypotension, bradycardia, hypothermia, and mortality, indicating the decisive involvement of reactive oxygen species (ROS) in these phenomena. Also, in classical TNF or lipopolysaccharide-induced shock models, tempol protected significantly. Experiments with (cell-permeable) superoxide dismutase or catalase, N-acetylcysteine and apocynin suggest that the ROS-dependent shock depends on intracellular center dot OH radicals. Potassium channels activated by ATP (K-ATP) or calcium (K-Ca) are important mediators of vascular relaxation. While NO and PGI2-induced vasodilation involves K-ATP and large-conductance BKCa channels, small-conductance SKCa channels mediate vasodilation induced by EDHF. Interestingly, also SKCa inhibition completely prevented the ROS-dependent shock. Our data thus indicate that intracellular center dot OH and SKCa channels represent interesting new therapeutic targets for inflammatory shock. Moreover, they may also explain why antioxidants other than tempol fail to provide survival benefit during shock.".
- aggregation authorList BK740977.
- aggregation endPage "930".
- aggregation issue "9".
- aggregation startPage "921".
- aggregation volume "88".
- aggregation aggregates 2937432.
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- aggregation similarTo s00109-010-0633-2.
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