Abstract
The present study was designed to investigate the efficacy of post-conditioning (POC) in the diabetic heart with myopathy (DCM) against ischaemia-reperfusion (I/R) injury in an isolated rat heart model. Present work includes three groups of male Wistar rat viz., (i) normal, (ii) diabetes mellitus (DM) and (iii) DCM and each group was subdivided into normal perfusion, I/R, and POC. Isolated heart from the rats was analysed for tissue injury, contractile function, mitochondrial function, and oxidative stress. Results demonstrated that unlike in DM heart and normal heart, POC procedure failed to recover the DCM heart from I/R induced cardiac dysfunction (measured via cardiac hemodynamics and infarct size. POC was unsuccessful in preserving mitochondrial subsarcolemmal fraction during I/R when compared with DM and normal heart. To conclude, the development of myopathy in diabetic heart abolished the cardioprotective efficacy of POC and the underlying pathology was linked with the mitochondrial dysfunction.
Early studies reported contradicting response of diabetic heart towards post-conditioning mediated cardioprotection.
Deteriorated mitochondrial function underlines the failure of post-conditioning in DCM.
Efficacy of cardioprotection depends on the varying pathology of different diabetes stages.
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Author contributions
Dr. Gino A Kurian has contributed to the design and implementation of the research, to the interpretation of the results and to the writing of the manuscript. Dr. Mahalakshmi and Mrs Priyanka have processed the experimental data, performed analysis, drafted the manuscript, designed figures & tables and compiled the literature sources.
Disclosure statement
The authors declare that they have no conflict of interest.
Data availability statement
The data that support the findings of this study are available from the corresponding author, [Dr. Gino A Kurian], upon reasonable request.