Cardiovascular effects of moderate-intensity static magnetic field exposure in experimental heart failure using a characterized exposure system.

BACKGROUND

Experimental findings on the biological effects of 0 Hz static magnetic fields (SMFs), representing the static component of the non-ionizing electromagnetic spectrum, remain inconsistent because of differences in field characteristics and exposure conditions. This study investigated the effects of moderate-intensity SMF exposure on cardiovascular and histopathological changes in an isoproterenol (ISO)-induced rat model of experimental heart failure (EHF) using a characterized system.

METHODS

Twenty-eight male Wistar rats were randomly assigned to four groups (Control, EHF, SMF, and EHF+SMF; n = 7/group). Experimental heart failure was induced by intraperitoneal ISO administration (5 mg/kg/day) for 7 consecutive days. Rats in the SMF and EHF+SMF groups were exposed to moderate-intensity SMF for 2 h/day, 5 days/week, for 21 days. The exposure system was characterized by two- and three-dimensional magnetic field mapping. Hemodynamics, electrocardiography, serum cardiac biomarkers (brain natriuretic peptide [BNP] and cardiac troponin T [cTnT]), and myocardial histopathology were evaluated.

RESULTS

Repeated ISO administration significantly reduced arterial pressure, produced selective electrocardiographic alterations, and induced myocardial inflammation and fibrosis. SMF exposure produced limited changes in hemodynamic, biochemical, and most electrocardiographic variables. Although BNP levels tended to decrease in the EHF+SMF group, neither BNP nor cTnT differed significantly from the untreated EHF group. In contrast, SMF exposure significantly reduced inflammatory cell infiltration, vascular congestion, and myocardial fibrosis.

CONCLUSION

Prolonged moderate-intensity SMF exposure had limited systemic cardiovascular effects but significantly reduced myocardial histopathological injury. These findings support further investigation of SMF exposure as a biophysical approach for modulating myocardial structural injury in experimental heart failure.