The effects of exposure of rats with a mild spinal cord injury to a 50 Hz magnetic field on general body condition, locomotion, pain, and secondary damages should be investigated.
Spinal cord injury was experimentally produced by surgical exposure and subsequent crushing of the spinal cord. Rats were divided into the following groups (n=6 each): 1) exposure of rats with spinal cord injury to the magnetic field, 2) spinal cord injury only (control group), 3) surgical exposure of spinal cord only, no injury (process control). A total of two rats from group 1 and one rat from group 2 died during the exposure procedure, and were therefore not included in the analysis. Exposure to the magnetic field started one day after surgery.
| Exposure | Parameters |
|---|---|
|
Exposure 1:
50 Hz
Exposure duration:
2 hours/day for 3 weeks
|
|
| Frequency | 50 Hz |
|---|---|
| Type | |
| Exposure duration | 2 hours/day for 3 weeks |
| Exposure source | |
|---|---|
| Chamber | polypropylene cages (50 × 20 × 15 cm3) |
| Setup | exposure system consisted of modified Helmholtz coils with 18 and 8 turns of wire wound on circular frames forming two outer and inner coils, respectively; rats were kept in cages in central area of the coils within a uniform magnetic field |
| Measurand | Value | Type | Method | Mass | Remarks |
|---|---|---|---|---|---|
| magnetic flux density | 17.96 µT | - | - | - | - |
Food intake was significantly decreased in the control group (group 2; only spinal cord injury) compared to the exposure group (group 1; spinal cord injury and magnetic field exposure) on day 5. Body weight did not show any significant differences between the groups. A significant improvement in bladder function and motor function was observed in group 1 compared to the control group. Histological analyses showed significantly higher tissue sparing at the injury epicenter and a significant decrease in calcium channel expression in group 1 compared to the control group.
The authors concluded that exposure to a 50 Hz magnetic field might promote sensory-motor recovery via attenuation of secondary damage and calcium-mediated excitotoxicity in rats with a mild spinal cord injury.
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