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Annals of Transplantation is one of the fast-developing journals open to all scientists and fields of transplant medicine and related research. The journal is published quarterly and provides extensive coverage of the most important advances in transplantation.
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Published: 2015-03-26

Preconditioning by Cilostazol Protects against Cold Hepatic Ischemia-Reperfusion Injury

Maximilian von Heesen, Simon Müller, Ulrich Keppler, Moritz J. Strowitzki, Claudia Scheuer, Martin K. Schilling, Michael D. Menger, Mohammed R. Moussavian

(Department of General, Vascular and Pediatric Surgery, University of Saarland, Homburg/Saar, Germany)

Ann Transplant 2015; 20:160-168

DOI: 10.12659/AOT.893031

Background: In liver transplantation, prolonged cold storage and post-transplant reperfusion are associated with endothelial inflammation, organ dysfunction, and graft failure. We herein studied whether cilostazol, a phosphodiesterase-3-inhibitor, attenuates post-ischemic liver injury after prolonged cold storage.
Material and Methods: Sprague-Dawley rats were assigned to 5 groups (n=6 each): sham animals (cold storage time (CST): 1 h), vehicle-treated (NaCl 0.9%) controls (CST: 24 h), and animals receiving 0.1, 1.0, or 10.0 mg/kg body weight (BW) cilostazol pre-treatment (CST: 24 h). After organ explantation, all livers were stored at 4°C in HTK solution, followed by 60 min of reperfusion with 37°C Krebs Henseleit buffer in a non-recirculating ex situ system. Bile flow was measured to evaluate liver function. To analyze inflammation and morphology, liver tissue samples were taken and histology, immunohistochemistry, and Western blotting were conducted.
Results: In vehicle-treated controls, prolonged cold storage and warm reperfusion induced inflammation, organ dysfunction, and cell death. This was indicated by an increase of hepatocellular vacuolization, endothelial ICAM-1 expression, and apoptotic cell death compared to sham animals. Cilostazol pre-treatment protected against cold hepatic ischemia-reperfusion injury by preventing hepatocellular disintegration, ICAM-1-associated endothelial inflammation, and apoptotic death.
Conclusions: Inhibition of PDE3 reduces endothelial cell activation and hepatocellular injury in cold ischemia/reperfusion of the liver.

Keywords: Cyclic AMP, Microcirculation, Organ Preservation, Reperfusion Injury

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DOI: 10.12659/AOT.892067

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Ganglong Gao, Zhenliang Sun, Liu Wenyong, Ye Dongxia, Runjia Zhao, Xueli Zhang

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DOI: 10.12659/AOT.892197