Original articles
DENG Weilin, ZHANG Chenjing, ZHANG Jing, PENG Ruiyun
Objective To investigate the dynamic changes in cardiac structure and function at different time points within one week following high-power microwave exposure in rats in order to provide data for formulating protective strategies and elucidating the mechanisms of microwave-induced cardiac injury. Methods Male Wistar rats were exposed to high-power microwave radiation in the S-band （2.856 GHz） at an average power density of 50 mW/cm² for 30 min. At 1, 3, and 7 days post-radiation, cardiac electrophysiological function, macroscopic morphology, and microscopic structure were assessed using serum biochemical analysis （the cardiac enzyme profile, injury markers, and ion concentrations）, electrocardiography （ECG）, echocardiography, hematoxylin-eosin （HE） staining, and transmission electron microscopy. Results Rectal temperatures significantly increased in rats after microwave irradiation. Biochemical results of the serum showed significant increases in levels of aspartate aminotransferase, lactate dehydrogenase, and creatine kinase at 1 and 7 days post-microwave exposure. Peak changes in fatty acid-binding protein, cardiac troponin T, N-terminal pro-B-type natriuretic peptide, and serum calcium and potassium ion concentrations occurred at 3 days post-exposure, indicating maximal injury at this time point. ECG revealed decreased heart rate, prolonged R-R intervals, and shortened corrected QT intervals at 1 day post-irradiation. Three days after exposure, heart rate increased and P-wave amplitude was elevated, but all parameters largely returned to control levels by day 7. Echocardiography suggested significant thickening of the interventricular septum and left ventricular wall, along with increased left ventricular mass starting at 3 days post-irradiation. These structural alterations persisted until day 7. Histopathological and ultrastructural observations confirmed that myocardial injury peaked at 3 days post-radiation, characterized by inflammatory cell infiltration, myofibrillar disarray, mitochondrial swelling and vacuolation, and disruption of sarcomere structure. These lesions were mitigated by day 7, but complete recovery did not occur. Conclusion 2.856 GHz high-power microwave radiation induces acute cardiac injury in rats, manifested as myocardial enzyme leakage, ion homeostasis imbalance, abnormal electrical activity, and tissue structural remodeling. The effect of injury occurs in a time-dependent manner and peaks at 3 days post-radiation. By day 7, there is partial recovery, yet residual structural abnormalities persist.
