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1 Biophysic, Hopital Widal, Laboratoire d'Etude de la Microcirculation, Paris, France
2 Laboratoire d'Anesthesie, Hopital de Bicetre, UPRES EA3540, Kremlin-Bicetre, France
* To whom correspondence should be addressed. E-mail: eric.vicaut{at}lrb.ap-hop-paris.fr.
In haemorrhagic shock, local hypoxia is present and followed by reoxygenation during the therapeutic process. In endothelium, reactive oxygen species (ROS) have been identified as a cause of inflammatory reactions and tissular lesions in ischemic territory during reoxygenation. This study was designed to identify the enzymatic mechanisms of ROS formation during reoxygenation after hypoxia. As severe shock, in vivo, can affect both O2 and nutriments, we combined hypoxia at a level close to that found in terminal vessels during shock, with glucose depletion, which induces a relevant additional stress. Human umbilical vein endothelial cells (HUVEC) underwent 2 hours of hypoxia (pO2~20mmHg) without glucose and one hour of reoxygenation (pO2~120mmHg) with glucose. ROS production was measured by the fluorescent marker 2',7'-dichlorodihydrofluorescein diacetate, and cell death, by propidium iodide. After one hour of reoxygenation, fluorescence had risen by 143 ± 17 %. Cell death was equal to 8.6 ± 2.4 %. Antimycin A, and stigmatellin, which inhibits the type III mitochondrial respiratory chain complex, reduced ROS production to values of 61 ± 10 % and 59 ± 7 % respectively, but inhibitors of other chain complexes did not affect it. Neither was the increase in fluorescence affected by inhibition of NADPH oxidase, xanthine oxidase, NO synthase, cyclo-oxygenase, cytochrome p450 monooxygenase, or monoamine oxidase. We did not observe any increase in cell death. These results show that in HUVEC, mitochondria are responsible for ROS production after hypoxia and reoxygenation, and suggest that a ROS release site is activated in the cytochrome b of the type III respiratory chain complex.
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