Fenofibrate ameliorates neural, mechanical, chemical, and electrical alterations in the murine model of heart failure. (October 2019)

• Record Type: Journal Article
• Authors: Dhyani, N; Saidullah, B; Fahim, M; Omanwar, S
• Is Part Of: Human & experimental toxicology. Volume 38:Number 10(2019)
• Page Start: 1183
• Page End: 1194
• Publication Date: 2019-10
• Subjects: Isoproterenol -- fenofibrate -- baroreflex sensitivity -- cardiac hypertrophy -- heart failure; Toxicology -- Periodicals; 615.9
• DOI: 10.1177/0960327119860173
• Languages: English
• ISSNs: 0960-3271

Abstract

Heart failure (HF) is a leading cause of hospitalization across the world and is known to cause ill-health and heavy economic losses. In the present study, a rat model of isoproterenol (ISO, 85 mg/kg subcutaneously for two subsequent days) induced HF was developed. ISO induces HF by its direct effect, that is, rise in left ventricular end-diastolic pressure (mechanical) and indirectly by altering the baroreflex (neural), electrocardiography (electrical), and development of oxidative stress and hyperlipidemia (chemical). Fenofibrate, a hypolipidemic drug, which ameliorates myocardial energy metabolism was seen to improve the both ISO-induced oxidative stress and lipid profile and consequently improved Baroreflex Sensitivity (BRS), partial ventricular functions, and cardiac hypertrophy. Therefore, our result suggests that fenofibrate treatment protected the heart by alleviating the ISO-induced effects, that is, neural, mechanical, electrical, and chemical alterations.