Cour 2011 Eur Heart J
Β» [[Has info::PMID: 20430770]]
Was written by::Cour M, Was written by::Loufouat J, Was written by::Paillard M, Was written by::Augeul L, Was written by::Goudable J, Was written by::Ovize M, Was written by::Argaud L (Was published in year::2011) Was published in journal::Eur Heart J
Abstract: [[has 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.]] β’ Keywords: has publicationkeywords::Cyclosporine A, has publicationkeywords::Cardiac arrest, has publicationkeywords::Cardiopulmonary resuscitation, has publicationkeywords::Ischaemia, has publicationkeywords::Reperfusion, has publicationkeywords::Pharmacological post-conditioning
Labels: MiParea: MiP area::Respiration, MiP area::mt-Medicine, MiP area::Pharmacology;toxicology
Stress:Injury and adaptation::Ischemia-reperfusion, Injury and adaptation::Permeability transition Organism: Organism::Rabbit Tissue;cell: tissue and cell::Heart Preparation: Preparation::Isolated mitochondria
Coupling state: Coupling states::LEAK, Coupling states::OXPHOS
Pathway: Pathways::N, Pathways::S
HRR: Instrument and method::Oxygraph-2k
An OROBOROS O2k was used in this publication, whereas the Anton Paar/OROBOROS Oxygraph was the first-generation instrument for high-resolution respirometry, which was replaced by the O2k in 2002.
- Further details: Gnaiger 2012 Abstract Bioblast-Gentle Science