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. 2017 Apr 5;12(4):e0174588.
doi: 10.1371/journal.pone.0174588. eCollection 2017.

Response of the human myocardium to ischemic injury and preconditioning: The role of cardiac and comorbid conditions, medical treatment, and basal redox status

Kelly Casós  1 , Gemma Ferrer-Curriu  1 , Paula Soler-Ferrer  1 , María L Pérez  1 , Eduard Permanyer  2 , Arnau Blasco-Lucas  2 , Juan Manuel Gracia-Baena  2 , Miguel A Castro  2 , Carlos Sureda  2 , Jordi Barquinero  3 , Manuel Galiñanes  1   2
Affiliations

Response of the human myocardium to ischemic injury and preconditioning: The role of cardiac and comorbid conditions, medical treatment, and basal redox status

Kelly Casós et al. PLoS One. .

Abstract

Background: 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.

Methods and results: 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.

Conclusions: 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.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Experimental protocol.
Tissues in all groups were equilibrated for 30–40 min at 37°C in aerobic conditions. Muscle tissues were either maintained under aerobic conditions (AC) for the entire experimental period or subjected to 90 min of ischemia followed by 120 min of ischemia/reoxygenation (I/R alone) or preconditioned (IPreC) with 5 min of ischemia and 5 min of reoxygenation.
Fig 2
Fig 2. Lactate dehydrogenase (LDH) leakage (A1) and 3-(4,5-dimethyl thiazol-2-yl)-2,5diphenyl tetrazolium bromide (MTT) reduction (B1) and the correlation between IPreC and I/R alone for LDH release (A2) and MTT reduction (B2) of human myocardium muscles (n = 300 per group) subjected to 250 min of aerobic condictions (AC), 90 min of ischemia followed by 120 min of reoxygenation (I/R alone), or ischemic preconditioning (IPreC) induced by 5 min of ischemia followed by 5 min of reoxygenation prior to the 90 min of ischemia.
The mean values are shown. *p < 0.05 vs AC group and †p < 0.05 vs I/R alone group.
Fig 3
Fig 3. Correlation between IPreC-I/R alone and I/R alone values for LDH release (A) and MTT reduction (B) in human myocardial muscles (n = 300), subjected to 90 min of normothemic ischemia followed by 120 min of reoxygenation (I/R alone) and ischemic preconditioning (IPreC) induced by 5 min of ischemia followed by 5 min of reoxygenation prior to the 90 min of ischemia.
*p < 0.05.
See this image and copyright information in PMC

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