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Eur J Cardiothorac Surg 2007;31:821-826. doi:10.1016/j.ejcts.2007.01.044
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Preclinical evaluation of coronary vascular function after cardioplegia with HTK and different antioxidant additives

^a Institute of Physiology, Medical Faculty Carl Gustav Carus, TU Dresden, Germany
^b Clinic of Anaesthesiology and Intensive Care Therapy, Medical Faculty Carl Gustav Carus, TU Dresden, Germany
^c Institute of Physiological Chemistry, University Hospital, Essen, Germany

Received 6 November 2006; received in revised form 23 January 2007; accepted 24 January 2007.

^_* Corresponding author. Address: Department of Physiology, Medical Faculty Carl Gustav Carus, TU Dresden, Fetscherstr. 74, D-01307 Dresden, Germany. Tel.: +49 351 458 6030; fax: +49 351 458 6301. (Email: Andreas.Deussen{at}mailbox.tu-dresden.de).

Objective: Due to limited resources, improvement of preservation solutions is still of great importance in cardiac transplant surgery. New additives with antioxidant properties were tested with respect to coronary function of isolated rat hearts. Methods: Bretschneider HTK solution containing none or an antioxidant additive (deferoxamine, trolox or LK 616) was used for 8 h cold cardioplegia. After reperfusion with Krebs-Henseleit buffer (KHB), we assessed vascular dilator capacity (bradykinin, adenosine triphosphate, reactive hyperemia), myocardial function (left ventricular developed pressure, heart rate, oxygen consumption) and release of biochemical markers (aspartate aminotransferase, creatine kinase, lactate dehydrogenase, troponin, adenosine). Results: Bradykinin- and adenosine triphosphate-induced vasodilations were largely reduced in hearts stored 8 h in traditional HTK as compared to unstored controls. Storage in HTK + LK 616 significantly improved bradykinin-induced vasodilation. Vasodilation toward ATP was best preserved in hearts stored in HTK + deferoxamine. Deferoxamine and trolox, both improved reactive hyperaemic response during reperfusion. Left ventricular pressure development was significantly reduced after 8 h cardioplegia, but no difference existed between different cardioplegia groups. Release of biochemical markers of tissue injury was similar in all cardioplegia groups. After storage in HTK + LK 616 (100 µM), however, heart marker release was slightly augmented as compared to HTK. Conclusions: Despite similar myocardial function and marker release, coronary vascular function after cardioplegic storage may profit by addition of iron chelators (or antioxidants) to traditional HTK solution.

Key Words: Coronary flow • Deferoxamine • Langendorff heart • LK 616 • Radical scavengers • Trolox