Difference between revisions of "Gnaiger 1999 Transplant Proc"
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{{Publication | {{Publication | ||
|title=Gnaiger E, Rieger G, Stadlmann S, Amberger A, Eberl T, Margreiter R (1999) Mitochondrial defect in endothelial cold ischemia/reperfusion injury. Transplant | |title=Gnaiger E, Rieger G, Stadlmann S, Amberger A, Eberl T, Margreiter R (1999) Mitochondrial defect in endothelial cold ischemia/reperfusion injury. Transplant Proc 31:994-5. | ||
|authors=Gnaiger | |info=[http://www.ncbi.nlm.nih.gov/pubmed/10083443 PMID: 10083443] | ||
|authors=Gnaiger Erich, Rieger G, Stadlmann S, Amberger A, Eberl T, Margreiter R | |||
|year=1999 | |year=1999 | ||
|journal=Transplant | |journal=Transplant Proc | ||
|abstract=ENDOTHELIAL ischemia/reperfusion injury is critical for organ preservation, yet the mechanisms of intracellular damage are little understood. Permeabilization of the cell membrane disrupts ion homeostasis, leading to secondary mitochondrial defects by influx of high extracellular Ca<sup>2+</sup> .<sup>1</sup> In contrast, primary mitochondrial damage is due to short-term (4 to 8-hour) cold ischemia/reoxygenation (CIR) of endothelial cells in University of Wisconsin (UW) or histidine-tryptophane-ketoglutarate (HTK) solution, while the cell membrane remains intact.<sup>2</sup> This study was designed to further characterize mitochondrial defects in CIR injury of endothelial cells. | |abstract=ENDOTHELIAL ischemia/reperfusion injury is critical for organ preservation, yet the mechanisms of intracellular damage are little understood. Permeabilization of the cell membrane disrupts ion homeostasis, leading to secondary mitochondrial defects by influx of high extracellular Ca<sup>2+</sup> .<sup>1</sup> In contrast, primary mitochondrial damage is due to short-term (4 to 8-hour) cold ischemia/reoxygenation (CIR) of endothelial cells in University of Wisconsin (UW) or histidine-tryptophane-ketoglutarate (HTK) solution, while the cell membrane remains intact.<sup>2</sup> This study was designed to further characterize mitochondrial defects in CIR injury of endothelial cells. | ||
| | |mipnetlab=AT Innsbruck Gnaiger E | ||
|discipline=Mitochondrial Physiology, Biomedicine | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Human | |||
|tissues=Endothelial;epithelial;mesothelial cell | |||
|preparations=Intact cells | |||
|injuries=Ischemia-reperfusion | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
Latest revision as of 04:25, 23 November 2021
| Gnaiger E, Rieger G, Stadlmann S, Amberger A, Eberl T, Margreiter R (1999) Mitochondrial defect in endothelial cold ischemia/reperfusion injury. Transplant Proc 31:994-5. |
Gnaiger Erich, Rieger G, Stadlmann S, Amberger A, Eberl T, Margreiter R (1999) Transplant Proc
Abstract: ENDOTHELIAL ischemia/reperfusion injury is critical for organ preservation, yet the mechanisms of intracellular damage are little understood. Permeabilization of the cell membrane disrupts ion homeostasis, leading to secondary mitochondrial defects by influx of high extracellular Ca2+ .1 In contrast, primary mitochondrial damage is due to short-term (4 to 8-hour) cold ischemia/reoxygenation (CIR) of endothelial cells in University of Wisconsin (UW) or histidine-tryptophane-ketoglutarate (HTK) solution, while the cell membrane remains intact.2 This study was designed to further characterize mitochondrial defects in CIR injury of endothelial cells.
• O2k-Network Lab: AT Innsbruck Gnaiger E
Labels:
Stress:Ischemia-reperfusion Organism: Human Tissue;cell: Endothelial;epithelial;mesothelial cell Preparation: Intact cells
Coupling state: OXPHOS
HRR: Oxygraph-2k
