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. 2009 Jul-Aug;41(6):2592-4.
doi: 10.1016/j.transproceed.2009.06.150.

Myocardial protection with the use of L-arginine and N-alpha-acetyl-histidine

A Koch  1 , T Radovits, S Loganathan, F-U Sack, M Karck, G B Szabó
Affiliations

Myocardial protection with the use of L-arginine and N-alpha-acetyl-histidine

A Koch et al. Transplant Proc. 2009 Jul-Aug.

Abstract

Objective: Effective myocardial preservation is an important condition for cardiac surgery, especially in heart transplantation with long ischemia times. During ischemia and reperfusion, myocardial function is altered by cold-induced ischemic injury. Cold-induced ischemic injury is triggered by cold storage and the amino acid histidine, a main component of the storage solution histidine-tryptophan-ketoglutarate (HTK). Cold-induced ischemic injury generates free oxygen radicals in an iron-dependent way. We investigated the efficacy of new modifications with the addition of L-arginine and N-alpha-acetyl-histidine to the well-established HTK solution (Custodiol) using a rat heart transplant model.

Materials and methods: Heterotopic transplantation was performed in Lewis rats (n = 20). After 1 hour of ischemic preservation and 1 hour of reperfusion, we assessed myocardial function and energy charge potential. The modifications of HTK solution included the addition of L-arginine, partial replacement of histidine with acetyl-histidine, and reduction of chloride concentration (HTK-1). In a second group, Custodiol served as the control.

Results: After 1 hour of reperfusion, left ventricular systolic pressure (106 +/- 33 vs 69 +/- 9 mm Hg; P < .05) and minimum rate of pressure development (dP/dt) (-1388 +/- 627 vs -735 +/- 219 mm Hg/s; P < .05) were significantly higher among the HTK-1 group compared with the control group. Energy charge potential did not differ significantly between the groups.

Conclusion: This study showed that the novel modified HTK-1 solution improved myocardial contractility and relaxation after heart transplantation.

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