Diabetic cardiomyopathy attenuated the protective effect of ischaemic post-conditioning against ischaemia-reperfusion injury in the isolated rat heart model

• Published in: Archives of physiology and biochemistry Vol. 129; no. 3; pp. 711 - 722
• Main Authors: Kurian, Gino A., Ansari, Mahalakshmi, Prem, Priyanka N.
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 04.05.2023
• Subjects: Animals; Diabetes Mellitus; Diabetic Cardiomyopathies; diabetic cardiomyopathy; Heart; Ischaemia-reperfusion injury; ischaemic post-conditioning; Ischemic Postconditioning - methods; Male; mitochondria; Myocardial Reperfusion Injury - pathology; Myocardial Reperfusion Injury - prevention & control; Rats; Rats, Wistar; ischaemic post-conditioning; Ischaemia-reperfusion injury; diabetic cardiomyopathy; mitochondria
• ISSN: 1381-3455; 1744-4160
• DOI: 10.1080/13813455.2020.1866017

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. KEY MESSAGES 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.