Difference between revisions of "Kuznetsov 2000 Transplant Proc"
Gnaiger Caro (talk | contribs) |
|||
| (2 intermediate revisions by 2 users not shown) | |||
| Line 2: | Line 2: | ||
|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=[http://www.ncbi.nlm.nih.gov/pubmed/10700961 PMID: 10700961] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/10700961 PMID: 10700961] | ||
|authors=Kuznetsov AV, Brandacher G, Steurer W, Margreiter R, Gnaiger | |authors=Kuznetsov AV, Brandacher G, Steurer W, Margreiter R, Gnaiger Erich | ||
|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> 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 | ||
}} | }} | ||
== Cited by == | |||
::* 5 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/10700961/ | |||
{{Labeling | {{Labeling | ||
|area=Respiration, mt-Medicine | |area=Respiration, mt-Medicine | ||
| Line 17: | Line 19: | ||
|diseases=Cardiovascular | |diseases=Cardiovascular | ||
|couplingstates=LEAK, OXPHOS | |couplingstates=LEAK, OXPHOS | ||
| | |pathways=N, S, CIV | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 14:16, 27 December 2021
| 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 Erich (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
Cited by
- 5 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/10700961/
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
