Difference between revisions of "Kuznetsov 2000 Transplant Proc"
Gnaiger Caro (talk | contribs) |
Beno Marija (talk | contribs) |
||
Line 17: | Line 17: | ||
|diseases=Cardiovascular | |diseases=Cardiovascular | ||
|couplingstates=LEAK, OXPHOS | |couplingstates=LEAK, OXPHOS | ||
| | |pathways=N, S, CIV | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} |
Revision as of 18:00, 7 November 2016
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
β’ O2k-Network Lab: AT Innsbruck Gnaiger E
Labels: MiParea: Respiration, mt-Medicine
Pathology: Cardiovascular
Stress:Ischemia-reperfusion
Organism: Rat
Tissue;cell: Heart
Preparation: Intact organ, Isolated mitochondria
Coupling state: LEAK, OXPHOS
Pathway: N, S, CIV
HRR: Oxygraph-2k