To test the hypothesis that pulsed electromagnetic fields increase the release of nitric oxide which influences vasodilation, microvascular perfusion and oxygen content in the brain of rats.
Pulsed electromagnetic fields could represent a promising therapy in stroke and traumatic brain injury. To evaluate this possibility, three groups of rats were examined: 1.) control group (n=5), 2.) exposure group (n=11) and 3.) exposure group + 10 mg (per kg body weight) of the nitric oxide synthase inhibitor L-NAME (n=7).
The rats were anesthetized and examined via a cranial window for four hours according to the following schedule: a) 30 minutes recording (baseline), b) 30 minutes recording (baseline), c) exposure (or no treatment in the control group), d) 30 minutes recording, e) 30 minutes brake, f) 30 minutes recording, g) 30 minutes brake and h) 30 minutes recording.
|Exposure duration||continuous for 30 minutes|
|Pulse width||3 ms|
|Repetition frequency||5 Hz|
|SAR||40 mW/kg||peak value||measured||-||measured in a phantom|
|electric field strength||6 V/m||-||-||-||± 1 V/m; within the rat brain|
After exposure (schedule point d and f), the diameter of arterioles and the red blood cell flow velocities increased significantly and the brain tissue oxygenation was significantly enhanced compared to the baselines recorded before, while these values were unchanged in the control group. At the end of the experiment (schedule point h), the changed parameters returned to those of the baseline. An administration of L-NAME prevented the exposure-induced effects which indicates an involvement of nitric oxide.
The authors conclude that pulsed electromagnetic fields increase microvascular cerebral blood flow via a nitric oxide dependent pathway. Hence, pulsed electromagnetic fields could represent an effective treatment in stroke and traumatic brain injuries.