Background: The later fate of a graft is highly dependent on its initial quality. Aside from
that the three predominant phases during transplantation (Tx) organ retrieval, cold static preservation
and reperfusion cause in a direct and indirect manner graft injury. There is complex ischemia
reperfusion injury (IRI) triggered during the whole process of Tx which contributes to further damage
of the graft.
Methods: The today's organ preservation with commercially available solutions that all have toxic potential
per se is still imperfect. Thus, improved preservation solutions are desperately needed to be able
to even safely preserve grafts from extended criteria donors which are more susceptible to especially
IRI. Most recently, a modified less toxic histidine-tryptophan-ketoglutarate (HTK; Custodiol®) the so
called histidine-tryptophan-ketoglutarate-N (HTK-N) for both better cardioplegia and organ preservation
for Tx has been developed. It is characterized as an electrolyte balanced, iron chelatorsupplemented,
and amino acid-fortified organ preservation solution with replaced buffer ameliorating
resistance to injury during the cold static preservation with subsequent IRI. Numerous in vitro and in
vivo experiments have shown the superiority of the HTK-N solution in ROS generation, microcirculation,
and subsequent inflammatory response compared with HTK.
Results: According to data available to date, HTK-N has both lower cytotoxicity and higher protective
potential than HTK. First clinical studies on both HTK-N for cardioplegia in cardiac surgery and for
organ preservation for transplantation have been performed or are ongoing.
Conclusion: In this review, the novelty and composition of HTK-N and studies investigating the potential
of this new solution are focussed, after summarizing the most relevant molecular mechanisms of