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J Thorac Cardiovasc Surg 2002;123:81-88
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Improved right heart function after myocardial preservation with 2,3-butanedione 2-monoxime in a porcine model of allogenic heart transplantation

Gregor Warnecke, Benjamin Schulze, Christian Hagl, MD, Axel Haverich, MD, Uwe Klima, MD

From the Department of Thoracic and Cardiovascular Surgery, Hannover Medical School, Hannover, Germany.

This work was supported in part by grants from the Hannover Medical School, Hannover, Germany.

Received for publication Jan 25, 2001. Revisions requested April 9, 2001; revisions received May 8, 2001. Accepted for publication June 8, 2001. Address for reprints: Uwe Klima, MD, PhD, Department of Thoracic and Cardiovascular Surgery, Hannover Medical School, 30623 Hannover, Germany (E-mail: klima{at}thg.mh-hannover.de).

Background: Right heart dysfunction is a major cause for early morbidity and mortality after heart transplantation. Experiments were designed to evaluate the influence of the calcium-desensitizing drug 2,3-butanedione 2-monoxime (BDM) on right heart function in a porcine model of heart transplantation.
Methods: Donor hearts of domestic pigs were arrested with BDM in Krebs solution (n = 7) and with BDM in Bretschneider's histidine-tryptophan-ketoglutarate (HTK) solution (n = 6). There were 2 control groups: University of Wisconsin (UW, n = 6) and HTK (n = 6). An isovolumic model was used in which the right ventricular volume was precisely controlled in vivo with an intracavitary high-compliance balloon. After 4 hours of ischemia, hearts were transplanted into recipients. After 1 and 2 hours of reperfusion, the right ventricular balloon volume was increased in 10-mL increments until right ventricular failure occurred and the developed pressures were recorded.
Results: Maximal right ventricular developed pressures were significantly different after 2 hours of reperfusion (UW: 35 ± 13 mm Hg; HTK: 47 ± 8 mm Hg; Krebs+BDM: 49 ± 9 mm Hg; HTK+BDM: 50 ± 6 mm Hg; P = .04). Hearts subjected to BDM could be loaded with a significantly increased volume after 1 hour and after 2 hours (UW: 57 ± 10 mL vs HTK: 43 ± 8 mL vs Krebs+BDM: 70 ± 10 mL vs HTK+BDM: 67 ± 15 mL; P = .002). Postischemic right ventricular enddiastolic compliance was significantly increased in groups treated with BDM after 1 hour (P = .02) and after 2 hours (P = .039).
Conclusions: The drug BDM significantly improves right ventricular function in a heart transplantation model. The increase in volume load and developed right ventricular pressure achieved by BDM application would translate into a decreased risk of right ventricular failure after clinical transplantation.




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