Introduction: Heat shock proteins (HSP) play essential roles in the synthesis, transport, and folding of proteins. During ischemia/reperfusion (I/R) injury to orthotopic liver transplants (OLT), disassembly of oligomeric complexes and unfolding of proteins are likely to occur, producing a major burden on HSP to prevent and/or reverse these events. To date, all studies have evaluated HSP expression in tissues after an I/R injury. No data are available on HSP serum levels during I/R injury in liver graft recipients.
Patients and methods: We evaluated the intraoperative and perioperative kinetics of HSP60 in the serum of 25 liver graft recipients.
Results: We observed a significant increase in serum levels of HSP60 at 4 hours compared with 30 minutes after reperfusion of the graft (P = .028). The perioperative HSP60 kinetics in serum neither correlated with the cold ischemia time nor the indocyanin green clearance. The type of preservation solution had no effect on serum HSP60 levels.
Conclusion: This first study provides evidence for increased serum levels of HSP60 after reperfusion in OLT. The perioperative kinetics of HSP60 in serum may result from suppressed protein synthesis caused by a reduced energy charge of hepatocytes during early reperfusion, impaired transcription, and/or corticosteroid treatment. Further studies are needed to clarify the role of HSP60 under clinical conditions including immunosuppressive medications in human OLT.
Copyright 2004 Elsevier Inc.