AI Summary & Key Takeaways
AI InsightThese findings suggest BMP-2 may serve as an ear-ly biomarker of cardiac remodeling in electrically active environments or device interfaces, such as pacemaker implantation zones.
📌 3 Key Takeaways
Abstract
Objective The 10 kV/m electric field, with a repetition frequency of 50 Hz and unidirectional pulsed (DC), which is accepted as the biological interaction limit by the World Health Organization, can also have an effect on cardiac tissues. 10 kV/m electric field exposure (pulsed wave shape) is increasingly seen both in the workplace and clinically. This study aimed to evaluate the structural and molecular responses of the heart to graded durations of 10 kV/m electric field (EF) exposure in rats. Material and Method Forty male Sprague-Dawley rats were randomly assigned to five groups (n = 8/group): control (0 min), and EF exposure for 1, 5, 15, or 30 minutes. Animals in the experimental groups were exposed to a pulsed electric field of 10 kV/m generated by a parallel-plate electrode system under standardized conditions.The pulses are unidirectional and have a repetition time of 20 ms (50 Hz). Hearts were harvested post-exposure and examined histopathologically. In addition, Bone Morphogenetic Protein-2 (BMP-2), vascular endothelial growth factor (VEGF), and fibroblast growth factor (FGF) immunohistochemical evaluation were performed, and immunopositivity was scored semi-quantitatively. Results Histopathological evaluation revealed intact myocardial architecture in control, 1-, 5-, and 15-minute groups. However, 30-minute EF exposure induced moderate hyperemia. Immunohistochemistry revealed minimal expression of BMP-2, VEGF, and FGF in early exposure groups, but BMP-2 showed focal upregulation in the 30 min group. VEGF and FGF remained unchanged. Conclusion Prolonged monophasic, high-intensity pulsed electric field exposure induces early signs of microvascular remodeling in cardiac tissue, reflected histologically by hyperemia and molecularly by increased BMP-2 expression. These findings suggest BMP-2 may serve as an ear-ly biomarker of cardiac remodeling in electrically active environments or device interfaces, such as pacemaker implantation zones.
Özet
Objective The 10 kV/m electric field, with a repetition frequency of 50 Hz and unidirectional pulsed (DC), which is accepted as the biological interaction limit by the World Health Organization, can also have an effect on cardiac tissues. 10 kV/m electric field exposure (pulsed wave shape) is increasingly seen both in the workplace and clinically. This study aimed to evaluate the structural and molecular responses of the heart to graded durations of 10 kV/m electric field (EF) exposure in rats. Material and Method Forty male Sprague-Dawley rats were randomly assigned to five groups (n = 8/group): control (0 min), and EF exposure for 1, 5, 15, or 30 minutes. Animals in the experimental groups were exposed to a pulsed electric field of 10 kV/m generated by a parallel-plate electrode system under standardized conditions.The pulses are unidirectional and have a repetition time of 20 ms (50 Hz). Hearts were harvested post-exposure and examined histopathologically. In addition, Bone Morphogenetic Protein-2 (BMP-2), vascular endothelial growth factor (VEGF), and fibroblast growth factor (FGF) immunohistochemical evaluation were performed, and immunopositivity was scored semi-quantitatively. Results Histopathological evaluation revealed intact myocardial architecture in control, 1-, 5-, and 15-minute groups. However, 30-minute EF exposure induced moderate hyperemia. Immunohistochemistry revealed minimal expression of BMP-2, VEGF, and FGF in early exposure groups, but BMP-2 showed focal upregulation in the 30 min group. VEGF and FGF remained unchanged. Conclusion Prolonged monophasic, high-intensity pulsed electric field exposure induces early signs of microvascular remodeling in cardiac tissue, reflected histologically by hyperemia and molecularly by increased BMP-2 expression. These findings suggest BMP-2 may serve as an ear-ly biomarker of cardiac remodeling in electrically active environments or device interfaces, such as pacemaker implantation zones.