https://doi.org/10.1140/epjs/s11734-026-02134-z
Regular Article
High-frequency pulsed electromagnetic field stimulation enhances cerebral microcirculation and tissue integrity after traumatic brain injury in rats
1
Lovelace Biomedical Research Institute, Albuquerque, NM, USA
2
Department of Neurological Diseases, Privolzhsky Research Medical University, Nizhny Novgorod, Russia
3
Department of Biology, Saratov State University, Saratov, Russia
4
Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, USA
5
Herzen Moscow Oncology Research Institute, A Branch of the National Medical Research Center of Radiology, Ministry of Health of Russia, Moscow, Russia
6
Lomonosov Moscow State University, Moscow, Russia
7
Department of Physiology, New York Medical College, Valhalla, NY, USA
a
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Received:
30
December
2025
Accepted:
10
January
2026
Published online:
23
March
2026
Abstract
Traumatic brain injury (TBI) induces microvascular dysfunction, tissue hypoxia, and blood–brain barrier (BBB) breakdown, driving secondary injury. High-frequency pulsed electromagnetic field (PEMF) stimulation is an emerging noninvasive “electroceutical” therapy that we have previously shown increases cerebral blood flow (CBF) and tissue oxygenation in the healthy rat brain. Here, we investigated whether acute PEMF could mitigate microvascular pathology in a rat TBI model. Male Sprague–Dawley rats underwent moderate fluid percussion injury (FPI) over the parietal cortex. Using in vivo two-photon laser scanning microscopy (2PLSM), we quantified peri-contusional arteriolar diameter, capillary red blood cell (RBC) velocity, microvascular shunt (MVS) flow, tissue oxygenation (NADH autofluorescence), and BBB permeability before and after a single 30-min PEMF (27.12 MHz, 3-ms bursts at 5 Hz, 6 V/m) or sham treatment. PEMF applied 1 h post-TBI significantly reversed pathological MVS flow (MVS/capillary ratio: 0.69 ± 0.06 vs. sham 0.90 ± 0.08, p < 0.01), increased capillary RBC velocity (86.3 ± 10.1% vs. sham 68.5 ± 9.8% of baseline, p < 0.05), and reduced tissue hypoxia (NADH: 115.2 ± 6.8% vs. sham 134.7 ± 10.2% of baseline, p < 0.05). BBB leakage was attenuated by ~ 35% (p < 0.01 vs. sham). These beneficial effects were abolished by pre-treatment with the NOS inhibitor L-NAME. Early neuronal death, assessed by propidium iodide staining 6 h post-TBI, was reduced in the PEMF group (19.8 ± 4.5% vs. sham 31.2 ± 5.7% PI + neurons, p < 0.05). We conclude that acute PEMF improves post-TBI microcirculation and confers neuroprotection via an NO-dependent mechanism that restores nutritive perfusion, limits hypoxia, and stabilizes the BBB.
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© The Author(s), under exclusive licence to EDP Sciences, Springer-Verlag GmbH Germany, part of Springer Nature 2026
Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
