Histomorphological and Physiological Assessment of Diabetic Cardiomyopathy in Rats

Abstract

Background: Diabetic cardiomyopathy is a major cardiovascular complication of diabetes mellitus characterized by structural and functional abnormalities of the myocardium independent of hypertension or coronary artery disease. Persistent hyperglycemia contributes to oxidative stress, inflammation, and impaired cardiac physiology, leading to progressive myocardial damage. This study aimed to perform a histological and physiological assessment of diabetic cardiomyopathy in streptozotocin-induced diabetic rats.

Methods: An experimental study was conducted in July-December 2025, on 20 adult male albino rats divided into two groups: control (n=10) and diabetic (n=10). Diabetes mellitus was induced by intraperitoneal injection of streptozotocin (55 mg/kg). Rats with fasting blood glucose levels ≥250 mg/dL after 72 hours were considered diabetic. After 8 weeks, physiological parameters including fasting blood glucose levels and myocardial thickness were evaluated. Heart tissues were collected and processed using standard histological techniques. Hematoxylin and eosin-stained sections were examined microscopically for myocardial fiber disorganization, cellular degeneration, edema, inflammatory infiltration, vascular congestion, hypertrophy, and fibrosis.

Results: Diabetic rats demonstrated significantly elevated fasting blood glucose levels (312.4 ± 28.6 mg/dL) compared to controls (96.8 ± 11.2 mg/dL) (p<0.001). Histological examination revealed marked myocardial abnormalities in diabetic rats, including myocardial fiber disorganization in 80% of specimens, cytoplasmic vacuolar degeneration in 70%, vascular congestion in 70%, interstitial edema in 60%, inflammatory infiltration in 50%, cardiomyocyte hypertrophy in 50%, and focal fibrosis in 40% of cases. Mean myocardial thickness was significantly increased in diabetic rats (18.6 ± 2.4 µm) compared to controls (12.9 ± 1.8 µm) (p=0.002). Fibrotic tissue area was also significantly higher in diabetic myocardium (16.3% ± 3.1%) than in controls (<3%) (p<0.001).

Conclusion: Diabetes mellitus induces significant histological and physiological alterations in myocardial tissue, resulting in structural degeneration, fibrosis, inflammation, and cardiac hypertrophy. These findings support the role of chronic hyperglycemia in the pathogenesis of diabetic cardiomyopathy and highlight the importance of early cardiovascular assessment in diabetes-related cardiac dysfunction.