Response of the human myocardium to ischemic injury and preconditioning

The diseased human myocardium is highly susceptible to ischemia/reoxygenation (I/R)-induced injury but its response to protective interventions such as ischemic preconditioning (IPreC) is unclear. Cardiac and other pre-existing clinical conditions as well as previous or ongoing medical treatment may...

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Detalles Bibliográficos
Autores: Casós, Kelly, Ferrer-Curriu, Gemma|||0000-0002-2651-649X, Soler-Ferrer, Paula, Pérez, María-Llanos, Permanyer, Eduard, Blasco-Lucas, Arnau|||0000-0002-2796-7428, Gracia Baena, Juan Manuel|||0000-0001-5277-3847, Castro, Miguel A., Sureda-Barbosa, Carlos, Barquinero Mañez, Jordi|||0000-0002-1677-9851, Galiñanes, Manuel|||0000-0002-0888-976X
Tipo de recurso: artículo
Fecha de publicación:2017
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:253857
Acceso en línea:https://ddd.uab.cat/record/253857
https://dx.doi.org/urn:doi:10.1371/journal.pone.0174588
Access Level:acceso abierto
Descripción
Sumario:The diseased human myocardium is highly susceptible to ischemia/reoxygenation (I/R)-induced injury but its response to protective interventions such as ischemic preconditioning (IPreC) is unclear. Cardiac and other pre-existing clinical conditions as well as previous or ongoing medical treatment may influence the myocardial response to I/R injury and protection. This study investigated the effect of both on myocardial susceptibility to I/R-induced injury and the protective effects of IPreC. Atrial myocardium from cardiac surgery patients (n = 300) was assigned to one of three groups: aerobic control, I/R alone, and IPreC. Lactate dehydrogenase leakage, as a marker of cell injury, and cell viability were measured. The basal redox status was determined in samples from 90 patients. The response to I/R varied widely. Myocardium from patients with aortic valve disease was the most susceptible to injury whereas myocardium from dyslipidemia patients was the least susceptible. Tissue from females was better protected than tissue from males. Myocardium from patients with mitral valve disease was the least responsive to IPreC. The basal redox status was altered in the myocardium from patients with mitral and aortic valve disease. The response of the myocardium to I/R and IPreC is highly variable and influenced by the underlying cardiac pathology, dyslipidemia, sex, and the basal redox status. These results should be taken into account in the design of future clinical studies on the prevention of I/R injury and protection.