THE EFFECTS OF COMBINATION OF RADIOFREQUENCY AND PULSED MAGNETIC FIELD ON CAROTID ARTERIA ISCHEMIA AND REPERFUSION INDUCED BRAIN INJURY: A PRELIMINARY REPORT

Abstract

Objective Cerebrovascular accident due to ischemia (IS) mediated by atherosclerotic plaque in the brain can trigger inflammation in the cerebral cortex, hippocampus and cerebellum tissues. Radiofrequency electromagnetic field (RF-EMF) and pulsed magnetic field (PMF) applications can increase nitric oxide formation from the vascular endothelial layer. The aim of this preliminary study is to reduce the damage caused by IS in different tissues of the brain by magnetic field applications. Material and Method A total of 9 rats, one rat in each group; sham, prophylactic RF, PMF, RF+PMF and therapeutic RF-EMF, PMF, RF-EMF+PMF, prophylactic and therapeutic RF-EMF+PMF and IS-only groups were distinguished. In single or combined applications of prophylactic/therapeutic RF-EMF and PMF groups, rats were taken to the experimental unit for 30 minutes of magnetic field exposure before and after 30 minutes of carotid artery occlusion for IS purposes. Histopathological hematoxylin-eosin staining in brain tissue (cerebral cortex and hippocampus) and cerebellum tissues taken after sacrification; With immunohistochemical analysis, brain derived neurotrophic factor (BDNF), tumor necrosis factoralpha (TNF-α), mammalian target of rapamycin (mTOR) and inducible nitric oxide synthase (iNOS) expressions were examined. Results Histopathologically significant hyperemia, edema, bleeding and neuronal degeneration were detected in the IS group. Additionally, immunohistochemically, an increase in TNF-α, mTOR, iNOS and a decrease in BDNF staining were observed. Prophylactic and/or therapeutic RF-EMF and/or PMF applications reversed all these parameters. The greatest improvement was observed in the Prophylactic+Therapeutic RFEMF+ PMF group. Conclusion As a result, the regression of IS-related inflammation in both brain tissue parts and cerebellar tissues with RFEMF and PMF is important in terms of the formation of neurological deficits, the continuity of learning and memory mechanisms, and the preservation of balance functions.