Electrocardiographic and histopathological characterizations of diabetic cardiomyopathy in rats.

Galal Yahya,Mahmoud E Youssef,Marwa A Abdel-Dayem,Ibtesam S Alanazi,Mona F El-Azab,Sameh Saber

doi:10.1007/s11356-021-17831-6

Abstract

Diabetes is a clinical condition that is associated with insulin deficiency and hyperglycemia. Cardiomyopathy, retinopathy, neuropathy, and nephropathy are well known complications of the elevated blood glucose. Diabetic cardiomyopathy is a clinical disorder that is associated with systolic and diastolic dysfunction along with cardiac fibrosis, inflammation, and elevated oxidative stress. In this study, diabetes was induced by intraperitoneal injection of streptozotocin (STZ) 50mg/kg. We determined the plasma levels of cardiac troponin-T (cTnT) and creatinine kinase MB (CK-MB) by ELISA. Diabetic rats showed abnormal cardiac architecture and increased collagen production. Significant elevation in ST-segment, prolonged QRS, and QT-intervals and increased ventricular rate were detected. Additionally, diabetic rats showed a prolongation in P wave duration and atrial tachyarrhythmia was observed. Plasma levels of cTnT and CK-MB were elevated. In conclusion, these electrocardiographic changes (elevated ST-segment, prolonged QT interval, and QRS complex, and increased heart rate) along with histopathological changes and increased collagen formation could be markers for the development of diabetic cardiomyopathy in rats.

Highlights

The defect in insulin formation and release leads to diabetes mellitus, which is characterized by an elevation in blood glucose levels
Prolonged hyperglycemia leads to macrovascular and microvascular damage leading to several complication, including retinopathy, nephropathy, neuropathy, and cardiomyopathy (Cole &Florez 2020)
The occurrence of diabetic cardiomyopathy is linked to several pathophysiological pathways, including the formation of advanced glycation end-products (AGEs), disturbances in microRNA, O-linked-Nacetylglucosamine and exosome (O-GlcNAc) pathways (Ducheix et al 2018), adenosine monophosphate (AMP)-activated protein kinase (AMPK) (Sun et al 2020), protein kinase C (PKC) (Yin et al 2019), and nuclear factor kappa B (NF-κB) formation (Fan et al 2018)

Summary

Introduction

The defect in insulin formation and release leads to diabetes mellitus, which is characterized by an elevation in blood glucose levels. Prolonged hyperglycemia leads to macrovascular and microvascular damage leading to several complication, including retinopathy, nephropathy, neuropathy, and cardiomyopathy (Cole &Florez 2020). Additional various metabolic disorders are accompanied with diabetic cardiomyopathy such as diminished nitric oxide levels, elevated oxidative stress, inflammation, and enhanced activity of renin-aldosterone angiotensin system (Tan et al 2020). The occurrence of diabetic cardiomyopathy is linked to several pathophysiological pathways, including the formation of advanced glycation end-products (AGEs), disturbances in microRNA, O-linked-Nacetylglucosamine and exosome (O-GlcNAc) pathways (Ducheix et al 2018), adenosine monophosphate (AMP)-activated protein kinase (AMPK) (Sun et al 2020), protein kinase C (PKC) (Yin et al 2019), and nuclear factor kappa B (NF-κB) formation (Fan et al 2018)

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