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Benedikt Preckel

Researcher at University of Amsterdam

Publications -  225
Citations -  5798

Benedikt Preckel is an academic researcher from University of Amsterdam. The author has contributed to research in topics: Perioperative & Ischemic preconditioning. The author has an hindex of 38, co-authored 206 publications receiving 4778 citations. Previous affiliations of Benedikt Preckel include Amsterdam University College & University of Düsseldorf.

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The influence of mitochondrial KATP-channels in the cardioprotection of preconditioning and postconditioning by sevoflurane in the rat in vivo.

TL;DR: The combination of preconditioning and postconditioning provides additive cardioprotection and is mediated, at least in part, by mKATP-channels.
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The noble gas xenon induces pharmacological preconditioning in the rat heart in vivo via induction of PKC-epsilon and p38 MAPK.

TL;DR: It is demonstrated that xenon induces cardioprotection by PC and that activation of PKC‐ɛ and its downstream target p38 MAPK are central molecular mechanisms involved.
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Molecular mechanisms transducing the anesthetic, analgesic, and organ protective actions of xenon

TL;DR: Clinical trials to assess the impact of xenon in settings with a high probability of injury such as cardiopulmonary bypass and neonatal asphyxia should be designed and underpinned with investigation of the molecular targets that transduce these effects.
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One MAC of sevoflurane provides protection against reperfusion injury in the rat heart in vivo

TL;DR: This investigation investigated whether the cardioprotection induced by sevoflurane against myocardial reperfusion injury was concentration-dependent and found it to be so, as to protect the heart against reperfusions.
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Remote ischemic conditioning to protect against ischemia-reperfusion injury: a systematic review and meta-analysis.

TL;DR: There is no evidence that remote ischemic conditioning reduces mortality associated with ischemia reperfusion events; nor does it reduce major adverse cardiovascular events; but it did reduce the incidence of peri-procedural myocardial infarctions, as well as the release of troponin.