Difference between revisions of "Kuznetsov 2000 Transplant Proc"
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|organism=Rat | |organism=Rat | ||
|tissues=Heart | |tissues=Heart | ||
|preparations=Intact | |preparations=Intact organ, Isolated mitochondria | ||
|injuries=Ischemia- | |injuries=Ischemia-reperfusion;preservation | ||
|diseases=Cardiovascular | |diseases=Cardiovascular | ||
|couplingstates=LEAK, OXPHOS | |couplingstates=LEAK, OXPHOS | ||
Revision as of 13:19, 13 February 2015
| Kuznetsov AV, Brandacher G, Steurer W, Margreiter R, Gnaiger E (2000) Isolated rat heart mitochondria and whole heart as models for mitochondrial cold ischemia-reperfusion injury. Transplant Proc 32:45. |
Kuznetsov AV, Brandacher G, Steurer W, Margreiter R, Gnaiger E (2000) Transplant Proc
Abstract: SHORT cold ischemia times (of less than 6 hours) tolerated by the heart remain one of the major problems in heart transplantation. Damaged mitochondria lead to heart injury by the diminished cellular energy status, oxidative stress, disturbance of ion balance, cytochrome c release, and induction of apoptosis.1-3 Improved understanding of preservation parameters affecting the efficiency of heart storage requires specific models of cold ischemia/reperfusion (CIR) injury.4
• O2k-Network Lab: AT_Innsbruck_Gnaiger E
Labels: MiParea: Respiration, mt-Medicine
Pathology: Cardiovascular
Stress:Ischemia-reperfusion;preservation"Ischemia-reperfusion;preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.
Organism: Rat
Tissue;cell: Heart
Preparation: Intact organ, Isolated mitochondria
Coupling state: LEAK, OXPHOS
HRR: Oxygraph-2k
