Histological and electrocardiographic assesment of chemically induced heart hypertrophy in mice

Aim: In the study, it was primarily aimed to create a cardiac hypertrophy model with Isoproterenol in mice. In this model, whether the '5-HT2B' serotonin receptor antagonist has a protective effect against myocardial hypertrophy and/or fibrosis was evaluated by vectorcardiographic and histological methods. Material and Methods: Four groups of Balb-C mice were formed, each receiving two of following drugs, saline (SF, sc), isoproterenol (ISO, 30 mg/kg/g, sc), and 5-HT2B antagonist (SER, 5 mg/kg/g, ip), for 15 days : i. SF+SF (control group: SFSF), ii. ISO+SF (ISOSF), iii. SER+ISO (SERISO), iv. SER+SF (SERSF). At 16th day, DII DIII leads digital ECG recordings were performed under Thiopental-Na anesthesia (50 mg/kg, ip). Frontal vectorcardiography (fVCG) was evaluated. Heart axes were measured at the beginning and end of ventricular depolarization (Ri and Rf). Cardiac hypertrophy was measured by the ratio of heart weight to body weight and the following histochemical stainings were performed: i. Masson trichrome, ii. HE, and iii. Immunohistochemical methods including Anti-ANP Anti-BNP natriuretic peptide receptor antibodies. Results: While there was no deviation in the Ri value, the Rf axis was higher in some mice in the ISOSF and SERISO groups. There was no difference in ECG interval measurements in any group. The JT segment was also elevated in some mice in the ISOSF and SERISO groups receiving isoproterenol, and the heart weight to body weight ratio significantly increased, as well. Intensive fibrosis was seen in ISOSF, whereas fibrosis in the SERISO group was less intense. Parallel to that both Anti-ANP and Anti-BNP immunoreactivities were significantly decreased. Conclusion: JT elevation in mice receiving isoproterenol is consistent with histological and immunohistological findings of fibrosis and hypertrophy. The reduction of these effects in the groups with the serotonin receptor antagonist '5-HT2B' indicates that fibrosis and hypertrophy are blocked. The activities of ANP and BNP receptors seems to be suppressed by the '5-HT2B' effect. Key words: Mice, Electrocardiography, Vectorcardiography, Isoproterenol, 5-HT2B, Cardiac hypertrophy