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Difference between revisions of "Kuznetsov 2000 Transplant Proc"

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{{Publication
{{Publication
|title=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.
|title=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.
|info=PMDI: 10700961
|info=[http://www.ncbi.nlm.nih.gov/pubmed/10700961 PMID: 10700961]
|authors=Kuznetsov AV, Brandacher G, Steurer W, Margreiter R, Gnaiger E
|authors=Kuznetsov AV, Brandacher G, Steurer W, Margreiter R, Gnaiger E
|year=2000
|year=2000
|journal=Transplant Proc
|journal=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.<sup>1-3</sup> Β  Improved understanding of preservation parameters affecting the efficiency of heart storage requires specific models of cold ischemia/reperfusion (CIR) injury.<sup>4</sup>
|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.<sup>1-3</sup> Improved understanding of preservation parameters affecting the efficiency of heart storage requires specific models of cold ischemia/reperfusion (CIR) injury.<sup>4</sup>
|mipnetlab=AT_Innsbruck_Gnaiger E
|mipnetlab=AT Innsbruck Gnaiger E
|discipline=Mitochondrial Physiology, Biomedicine
|discipline=Mitochondrial Physiology, Biomedicine
}}
}}
{{Labeling
{{Labeling
|area=Respiration, mt-Medicine
|organism=Rat
|tissues=Heart
|preparations=Intact organ, Isolated mitochondria
|injuries=Ischemia-reperfusion
|diseases=Cardiovascular
|couplingstates=LEAK, OXPHOS
|pathways=N, S, CIV
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|injuries=Ischemia-Reperfusion; Preservation
|organism=Rat
|tissues=Cardiac muscle
|preparations=Intact Organ, Isolated Mitochondria
|couplingstates=OXPHOS
|discipline=Mitochondrial Physiology, Biomedicine
|discipline=Mitochondrial Physiology, Biomedicine
}}
}}

Revision as of 17:00, 7 November 2016

Publications in the MiPMap
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.

Β» PMID: 10700961

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