Monotherapy of experimental metabolic syndrome: II. Study of cardiovascular effects

• Published in: Interdisciplinary toxicology Vol. 10; no. 3; pp. 86 - 92
• Main Authors: Knezl, Vladimír, Sotníková, Ružena, Brnoliaková, Zuzana, Stankovičová, Tatiana, Bauer, Viktor, Bezek, Štefan
• Format: Journal Article
• Language: English
• Published: Slovakia De Gruyter Open 01.11.2017; De Gruyter Poland; Slovak Toxicology Society SETOX
• Subjects: Antioxidants; Aorta; Atorvastatin; Blood pressure; Cardiovascular diseases; cardiovascular effects; Cardiovascular system; Cholesterol; Coronary vessels; Diet; Echocardiography; EKG; Endothelium; Health risks; Heart diseases; High cholesterol diet; High fat diet; high-fat and high-cholesterol diet; Metabolic syndrome; Myocardium; Original; Rats; Risk analysis; Risk factors; Rodents; SMe1EC2; metabolic syndrome; high-fat and high-cholesterol diet; atorvastatin; SMe1EC2; cardiovascular effects
• DOI: 10.1515/intox-2017-0014
• ISSN: 1337-6853; 1337-9569

Metabolic syndrome belongs to the most important risk factors of cardiovascular diseases. The aim of this study was to investigate changes in cardiovascular system induced by high cholesterol and high fat diet (HCHF) in HTG rats and their influence by a pyridoindole antioxidant – SMe1EC2 (S). The effects of S were compared with those of atorvastatin (A). Male HTG rats were fed HCHF (1% cholesterol + 7.5% lard) for 4 weeks. S and A were administered p.o., 50 mg/kg b.w. Following experimental groups were used: Wistar rats (W), hypertriglyceridemic rats (HTG), HTG rats fed HCHF (CHOL), HTG+S (S-HTG), CHOL+S (S-CHOL), and CHOL+A (A-CHOL). Values of blood pressure (BP) and selected ECG parameters were monitored in conscious animals, functions of the isolated heart and aorta were analyzed . At the end of the experiment, systolic (sBP) and diastolic (dBP) blood pressure was increased in HTG and CHOL. S and A decreased BP in all treated groups. Accordingly with BP changes, the aortic endothelial function of CHOL was damaged. Both S and A administration ameliorated the endothelium-dependent relaxation to values of W. PQ and QTc intervals were prolonged in CHOL, while the treatment with S or A improved ECG findings. Prodysrhythmogenic threshold was decreased significantly in CHOL and both treatments returned it to the control values. In conclusion, HCHF increased BP, impaired endothelial relaxation of the aorta and potentiated susceptibility of myocardium to dysrhythmias. The effect of S on the changes induced by HCHF diet was more pronounced than that of A.