Cardioprotective effects of L-arginine in a mesatone-induced rat model of chronic heart failure: biochemical and electrocardiographic insights

The management of chronic heart failure (CHF) remains a critical challenge in cardiovascular pathology. This study aimed to investigate the role of L-arginine in a mesatone-induced rat model of CHF. L-arginine exhibits cardioprotective effects. CHF was induced in experimental groups by intramuscular administration of 0.1 mL of a 1 % mesatone solution, followed by daily free swimming until profound fatigue for 21 days. The experiment continued until stable and irreversible myocardial changes developed. One experimental group received L-arginine at a dose of 20 mg/kg intraperitoneally for 10 days. The control group consisted of intact animals. The impact of CHF on the cardiovascular system was assessed through biochemical and electrocardiographic (ECG) parameters. In CHF-induced rats, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels increased by 36.7 % (P ≤ 0.05) and 184.1 % (P ≤ 0.05), respectively, compared to the control group. Additionally, CHF was associated with an increase in creatinine levels by 152.6 % (P ≤ 0.01) and urea levels by 207.0 % (P ≤ 0.05), indicating renal dysfunction. Electrolyte imbalances included elevated sodium, potassium, and chloride levels, reflecting the activation of the renin-angiotensin-aldosterone system (RAAS). CHF also caused significant alterations in ECG parameters, including a 24.8 % (P ≤ 0.05) reduction in heart rate, a 50.2 % (P ≤ 0.05) decrease in R-wave amplitude, and a 192.9 % (P ≤ 0.05) reduction in T-wave amplitude. Additionally, CHF led to a 37.2 % (P ≤ 0.05) prolongation of the QRS complex and a 60.3 % (P ≤ 0.05) increase in QT interval duration, indicating myocardial conduction abnormalities and impaired ventricular repolarization. L-arginine administration demonstrated a cardioprotective effect by reducing AST levels by 27.7 % (P ≤ 0.05) and ALT by 5.8 %, suggesting improved myocardial function. Furthermore, creatinine and urea levels decreased by 46.9 % (P ≤ 0.05) and 60.0 % (P ≤ 0.05), respectively, indicating a beneficial effect on renal function. Electrolyte imbalances were partially corrected, with potassium levels decreasing by 69.9 % (P ≤ 0.05) and chloride levels by 44.1 % (P ≤ 0.05). L-arginine also contributed to the partial normalization of ECG parameters, leading to a 9.0 % (P ≤ 0.05) increase in heart rate, reduction in QT interval prolongation, and improved ventricular conduction. These findings suggest that L-arginine mitigates biochemical and electrophysiological disturbances associated with CHF, supporting its potential as a cardioprotective agent.