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Verfasst von:Berger, Marc Moritz [VerfasserIn]   i
 Huhn-Wientgen, Ragnar [VerfasserIn]   i
 Oei, Gezina T. [VerfasserIn]   i
 Heinen, André [VerfasserIn]   i
 Winzer, Andreas [VerfasserIn]   i
 Bauer, Inge [VerfasserIn]   i
 Preckel, Benedikt [VerfasserIn]   i
 Weber, Nina Claudia [VerfasserIn]   i
 Schlack, Wolfgang [VerfasserIn]   i
 Hollmann, Markus W. [VerfasserIn]   i
Titel:Hypoxia induces late preconditioning in the rat heart in vivo
Verf.angabe:Marc M. Berger, M.D., Ragnar Huhn, M.D., Ph.D., Gezina T. Oei, B.Sc., M.Sc., André Heinen, M.D., Ph.D., Andreas Winzer, M.D., Inge Bauer, Ph.D., Benedikt Preckel, M.D., M.A., D.E.A.A., Nina C. Weber, Ph.D., Wolfgang Schlack, M.D., D.E.A.A., Markus W. Hollmann, M.D., Ph.D., D.E.A.A.
E-Jahr:2010
Jahr:December 2010
Umfang:10 S.
Fussnoten:Gesehen am 18.01.2023
Titel Quelle:Enthalten in: Anesthesiology
Ort Quelle:Hagerstown, Md. : Lippincott Williams & Wilkins, 1940
Jahr Quelle:2010
Band/Heft Quelle:113(2010), 6, Seite 1351-1360
ISSN Quelle:1528-1175
Abstract:Although hypoxic late preconditioning (LPC) limits ischemia-reperfusion injury in vitro, its cardioprotective effect is not established in vivo.In part 1, rats were exposed to 4 h of hypoxia (16%, 12%, 8% oxygen) before 24 h of reoxygenation. In part 2, normoxic rats received early preconditioning with sevoflurane (1 minimum alveolar concentration [MAC] for 3 × 5 min), continuous administration of 1 MAC sevoflurane, or 11 mg · kg · h propofol. Thereafter, all rats underwent 25 min of regional myocardial ischemia and 120 min of reperfusion. After reperfusion, hearts were excised for infarct staining. The expression of protein kinase C (PKC)α and PKCε was assessed by Western blot analysis and the expression of heme oxygenase-1 and vascular endothelial growth factor by reverse transcriptase polymerase chain reaction.In normoxic control rats, infarct size was 62 ± 6% of the area at risk. Hypoxic LPC reduced infarct size (LPC16: 36 ± 11%, LPC12: 38 ± 10%, LPC8: 39 ± 11%; each P < 0.001) to approximately the same magnitude as sevoflurane-preconditioning (40 ± 8%; P < 0.001). Combined LPC16 and sevoflurane preconditioning was not superior to either substance alone. Continuous sevoflurane or propofol was not protective. The PKC inhibitor calphostin C abolished the cardioprotective effects of LPC16. PKCε, but not PKCα, expression was increased 6 and 28 h after hypoxic LPC. Heme oxygenase-1 and vascular endothelial growth factor were transiently up-regulated after 6 h.Hypoxic LPC at 8%, 12%, and 16% oxygen reduces infarct size in the rat heart in vivo. This effect is as powerful as sevoflurane-preconditioning. PKCε is a key player in mediating hypoxic LPC.
DOI:doi:10.1097/ALN.0b013e3181fce7ea
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1097/ALN.0b013e3181fce7ea
 DOI: https://doi.org/10.1097/ALN.0b013e3181fce7ea
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1831425564
Verknüpfungen:→ Zeitschrift

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