Mitochondrial defects by intracellular calcium overload versus endothelial cold ischemia/reperfusion injury.

@article{Gnaiger2000MitochondrialDB,
  title={Mitochondrial defects by intracellular calcium overload versus endothelial cold ischemia/reperfusion injury.},
  author={Erich Gnaiger and A. V. Kuznetsov and Gunde Rieger and Albert Amberger and Annette Maria Fuchs and Sylvia Stadlmann and Thomas Eberl and Raimund Margreiter},
  journal={Transplant international : official journal of the European Society for Organ Transplantation},
  year={2000},
  volume={13 Suppl 1},
  pages={S555-7}
}
Questions as to the critical stress factor and primary targets of cold ischemia/reperfusion (CIR) injury were addressed by comparing mitochondrial defects caused by (1) CIR injury and (2) intracellular Ca2+ overload. CIR was simulated in transformed human umbilical vein endothelial cell cultures (tEC) by 8 h cold anoxia in University of Wisconsin solution and reoxygenation at 37 degrees C. Intracellular Ca2+ concentrations were changed by permeabilization of suspended cells with digitonin in… CONTINUE READING