Difference between revisions of "Cour 2011 Eur Heart J"
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{{Publication | {{Publication | ||
|title=Cour M, Loufouat J, Paillard M, Augeul L, Goudable J, Ovize M, Argaud L (2011) Inhibition of mitochondrial permeability transition to prevent the post-cardiac arrest syndrome: a pre-clinical study. Eur Heart J 32:226-35. | |title=Cour M, Loufouat J, Paillard M, Augeul L, Goudable J, Ovize M, Argaud L (2011) Inhibition of mitochondrial permeability transition to prevent the post-cardiac arrest syndrome: a pre-clinical study. Eur Heart J 32:226-35. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20430770 PMID: 20430770] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/20430770 PMID: 20430770] | ||
|authors=Cour M, Loufouat J, Paillard M, Augeul L, Goudable J, Ovize M, Argaud L | |authors=Cour M, Loufouat J, Paillard M, Augeul L, Goudable J, Ovize M, Argaud L | ||
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|tissues=Heart | |tissues=Heart | ||
|preparations=Isolated mitochondria | |preparations=Isolated mitochondria | ||
|injuries=Ischemia-reperfusion | |injuries=Ischemia-reperfusion | ||
|couplingstates=LEAK, OXPHOS | |couplingstates=LEAK, OXPHOS | ||
|substratestates=CI, CII | |substratestates=CI, CII | ||
Revision as of 08:28, 16 June 2015
| Cour M, Loufouat J, Paillard M, Augeul L, Goudable J, Ovize M, Argaud L (2011) Inhibition of mitochondrial permeability transition to prevent the post-cardiac arrest syndrome: a pre-clinical study. Eur Heart J 32:226-35. |
Cour M, Loufouat J, Paillard M, Augeul L, Goudable J, Ovize M, Argaud L (2011) Eur Heart J
Abstract: Resuscitated cardiac arrest (CA), leading to harmful cardiovascular dysfunction and multiple organ failure, includes a whole-body hypoxia-reoxygenation phenomenon. Opening of the mitochondrial permeability transition pore (mPTP) appears to be a pivotal event in ischaemia-reperfusion injury. We hypothesized that pharmacological inhibition of mPTP opening may prevent the post-CA syndrome.
Anaesthetized New Zealand White rabbits underwent a 15 min primary asphyxial CA and 120 min of reperfusion following resuscitation. At reflow, animals received an intravenous bolus of either cyclosporine A (CsA, 5 mg/kg) or NIM 811 (2.5 mg/kg), two potent inhibitors of mPTP opening, or the CsA vehicle (control). Short-term survival, haemodynamics, regional (sonomicrometry), and global cardiac function (dP/dt and aortic flow) were assessed. We measured markers of cellular injuries and/or organ failure, including troponin Ic release, lacticodehydrogenase, lactate, creatinine, and alanine aminotransferase. Cyclosporine A and NIM 811 significantly improved short-term survival, post-resuscitation cardiac function, as well as liver and kidney failure (P < 0.05). CsA and NIM 811 both attenuated in vitro mPTP opening (calcium retention capacity by spectrofluorimetry) and restored oxidative phosphorylation when compared with controls (P < 0.05).
These data suggest that pharmacological inhibition of mPTP opening, added to basic life support, attenuates the post-CA syndrome and improves short-term outcomes in the rabbit model. • Keywords: Cyclosporine A, Cardiac arrest, Cardiopulmonary resuscitation, Ischaemia, Reperfusion, Pharmacological post-conditioning
Labels: MiParea: Respiration, Pharmacology;toxicology
Stress:Ischemia-reperfusion Organism: Rabbit Tissue;cell: Heart Preparation: Isolated mitochondria
Coupling state: LEAK, OXPHOS
HRR: Oxygraph-2k
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