Non-heart-beating donor porcine livers: the adverse effect of cooling.
Normothermic preservation has been shown to be advantageous in an experimental model of preservation of non-heart-beating donor (NHBD) livers, which have undergone significant warm ischemic injury. The logistics of clinical organ retrieval might dictate a period of cold preservation prior to warm perfusion. We have investigated the effects of a brief period of cold preservation on NHBD livers prior to normothermic preservation. Porcine livers were subjected to 60 minutes of warm ischaemia and then assigned to following groups: Group W (n = 5), normothermic preservation for 24 hours; and Group C (n = 6), cold preservation in University of Wisconsin solution for 1 hour followed by normothermic preservation for 23 hours (total preservation time, 24 hours). Synthetic function (bile production and factor V production) and cellular damage were compared on the ex vivo circuit during preservation. There was no significant difference in the synthetic function of the livers (bile production and factor V production). Markers of hepatocellular damage (alanine aminotransferase and aspartate aminotransferase release), sinusoidal endothelial cell dysfunction (hyaluronic acid), and Kupffer cell injury (beta-galactosidase) were significantly higher in Group C. The histology of the livers at the end of perfusion was similar. In conclusion, a brief-period cold preservation prior to normothermic perfusion maintains the synthetic function and metabolic activity but results in significant hepatocellular damage, sinusoidal endothelial cell dysfunction, and Kupffer cell injury. Transplant studies are required to establish whether livers treated in this way are viable for transplantation.
Reddy
Srikanth
S
Nuffield Department of Surgery, University of Oxford, Oxford, OX3 9DU, UK.
Greenwood
Joanne
J
Maniakin
Nikolai
N
Bhattacharjya
Shantanu
S
Zilvetti
Miguel
M
Brockmann
Jens
J
James
Tim
T
Pigott
David
D
Friend
Peter
P
D000818:Animals; D001646:Bile / Q000378:metabolism; D003080:Cold Temperature / Q000009:adverse effects*; D042783:Endothelial Cells / Q000473:pathology; D005165:Factor V / Q000378:metabolism; D005697:Galactosides / Q000378:metabolism; D006085:Graft Survival; D006323:Heart Arrest; D008099:Liver / Q000473:pathology / Q000502:physiology; D016031:Liver Transplantation; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D034421:Sus scrofa
D005697:Galactosides; C007816:beta-galactoside; D005165:Factor V