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Canadian Journal of Gastroenterology and Hepatology
Volume 2019, Article ID 5683479, 11 pages
Research Article

Ischemic Postconditioning (IPostC) Protects Fibrotic and Cirrhotic Rat Livers after Warm Ischemia

1Berlin Institute of Health Charité – Universitätsmedizin Berlin, Germany
2Department of Pathology, University of Munich, Campus Grosshadern, Munich, Germany
3Department of Medicine II, University Hospital, Liver Centre Munich, LMU Munich, Germany
4Department of Surgery, University of Munich, Campus Grosshadern, Munich, Germany
5Division of Clinical Pharmacology, University of Munich, Campus Innenstadt, Munich, Germany

Correspondence should be addressed to Christian J. Steib; ed.nehcneum-inu.dem@biets.naitsirhc

Received 29 December 2018; Revised 14 May 2019; Accepted 19 May 2019; Published 9 June 2019

Academic Editor: Quirino Lai

Copyright © 2019 Julia Schewe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Decreased organ function following liver resection is a major clinical issue. The practical method of ischemic postconditioning (IPostC) has been studied in heart diseases, but no data exist regarding fibrotic livers. Aims. We aimed to determine whether IPostC could protect healthy, fibrotic, and cirrhotic livers from ischemia reperfusion injury (IRI). Methods. Fibrosis was induced in male SD rats using bile duct ligation (BDL, 4 weeks), and cirrhosis was induced using thioacetamide (TAA, 18 weeks). Fibrosis and cirrhosis were histologically confirmed using HE and EvG staining. For healthy, fibrotic, and cirrhotic livers, isolated liver perfusion with 90 min of warm ischemia was performed in three groups (each with n=8): control, IPostC 8x20 sec, and IPostC 4x60 sec. additionally, healthy livers were investigated during a follow-up study. Lactate dehydrogenase (LDH) and thromboxane B2 (TXB2) in the perfusate, as well as bile flow (healthy/TAA) and portal perfusion pressure, were measured. Results. LDH and TXB2 were reduced, and bile flow was increased by IPostC, mainly in total and in the late phase of reperfusion. The follow-up study showed that the perfusate derived from a postconditioned group had much less damaging potential than perfusate derived from the nonpostconditioned group. Conclusion. IPostC following warm ischemia protects healthy, fibrotic, and cirrhotic livers against IRI. Reduced efflux of TXB2 is one possible mechanism for this effect of IPostC and increases sinusoidal microcirculation. These findings may help to improve organ function and recovery of patients after liver resection.