Endothelial dysfunction of bypass graft

• Verfasst von: Veres, Gábor [VerfasserIn]
• Verfasst von: Hegedűs, Péter [VerfasserIn]
• Verfasst von: Barnucz, Enikő [VerfasserIn]
• Verfasst von: Zöller, Raphael [VerfasserIn]
• Verfasst von: Klein, Stephanie [VerfasserIn]
• Verfasst von: Schmidt, Harald [VerfasserIn]
• Verfasst von: Radovits, Tamás [VerfasserIn]
• Verfasst von: Korkmaz-İçöz, Sevil [VerfasserIn]
• Verfasst von: Karck, Matthias [VerfasserIn]
• Verfasst von: Szabó, Gábor [VerfasserIn]
• Titel: Endothelial dysfunction of bypass graft
• Titelzusatz: direct comparison of in Vitro and in vivo models of ischemia-reperfusion injury
• Verf.angabe: Gábor Veres, Péter Hegedűs, Enikő Barnucz, Raphael Zöller, Stephanie Klein, Harald Schmidt, Tamás Radovits, Sevil Korkmaz, Matthias Karck, Gábor Szabó
• E-Jahr: 2015
• Jahr: April 15, 2015
• Umfang: 13 S.
• Fussnoten: Gesehen am 09.07.2020
• Titel Quelle: Enthalten in: PLOS ONE
• Ort Quelle: San Francisco, California, US : PLOS, 2006
• Jahr Quelle: 2015
• Band/Heft Quelle: 10(2015,4) Artikel-NUmmer e0124025, 13 Seiten
• ISSN Quelle: 1932-6203
• DOI: doi:10.1371/journal.pone.0124025
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Coronary artery bypass grafting
• Sach-SW: Endothelial cells
• Sach-SW: Endothelium
• Sach-SW: Gene expression
• Sach-SW: Hypochlorites
• Sach-SW: Ischemia
• Sach-SW: Reperfusion
• Sach-SW: Reperfusion injury
• K10plus-PPN: 1722617837

Abstract

Background Although, ischemia/reperfusion induced vascular dysfunction has been widely described, no comparative study of in vivo- and in vitro-models exist. In this study, we provide a direct comparison between models (A) ischemic storage and in-vitro reoxygenation (B) ischemic storage and in vitro reperfusion (C) ischemic storage and in-vivo reperfusion. Methods and Results Aortic arches from rats were stored for 2 hours in saline. Arches were then (A) in vitro reoxygenated (B) in vitro incubated in hypochlorite for 30 minutes (C) in vivo reperfused after heterotransplantation (2, 24 hours and 7 days reperfusion). Endothelium-dependent and independent vasorelaxations were assessed in organ bath. DNA strand breaks were assessed by TUNEL-method, mRNA expressions (caspase-3, bax, bcl-2, eNOS) by quantitative real-time PCR, proteins by Western blot analysis and the expression of CD-31 by immunochemistry. Endothelium-dependent maximal relaxation was drastically reduced in the in-vivo models compared to ischemic storage and in-vitro reperfusion group, and no difference showed between ischemic storage and control group. CD31-staining showed significantly lower endothelium surface ratio in-vivo, which correlated with TUNEL-positive ratio. Increased mRNA and protein levels of pro- and anti-apoptotic gens indicated a significantly higher damage in the in-vivo models. Conclusion Even short-period of ischemia induces severe endothelial damage (in-vivo reperfusion model). In-vitro models of ischemia-reperfusion injury can be limitedly suited for reliable investigations. Time course of endothelial stunning is also described.