Effects of brain death and hemodynamic status on function and immunologic activation of the potential donor liver in the rat

JAB van der Hoeven*, GJ Ter Horst, G Molema, P de Vos, ARJ Girbes, F Postema, RL Freund, J Wiersema, R van Schilfgaarde, RJ Ploeg

*Corresponding author voor dit werk

OnderzoeksoutputAcademicpeer review

134 Citaten (Scopus)

Samenvatting

Objective

To assess the effect on the function and immunologic status of potential donor livers of the duration of brain death combined with the presence and absence of hemodynamic instability in the donor.

Summary Background Data

Brain death, regarded as a given condition in organ transplantation, could have significant effects on the donor organ quality.

Methods

Brain death was induced in Wistar rats. Short or long periods of brain death in the presence or absence of hemodynamic instability were applied. Sham-operated rats served as controls. Organ function was studied by monitoring standard serum parameters. The inflammatory status of the liver was assessed by determining the immediate early gene products, the expression of cell adhesion molecules, and the influx of leukocytes in the liver.

Results

Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors. Irrespective of hemodynamic status, a progressive inflammatory activation could be observed in brain-dead rats compared with controls.

Conclusions

Brain death causes progressive liver dysfunction, which is made worse by the coexistence of hemodynamic instability. Further, brain death activates the inflammatory status of the potential donor liver. irrespective of the presence of hypotension. The changes observed may predispose the graft to additional damage from ischemia and reperfusion in the transplant procedure.

Originele taal-2English
Pagina's (van-tot)804-812
Aantal pagina's9
TijdschriftAnnals of Surgery
Volume232
Nummer van het tijdschrift6
StatusPublished - dec.-2000
Evenement7th Annual Meeting of the European-Surgical-Association - , Netherlands
Duur: 14-apr.-200015-apr.-2000

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