Diabetes mellitus is associated with impairments of vascular responsiveness to neurotransmitters. Pulsed electromagnetic fields induce small electrical currents within the body that can cause depolarization, repolarization and hyperpolarization in neurons. It was hypothesized that this could potentially modulate neuronal activity and related vascular responses in rats.
Male rats were divided into four groups (each n=15): 1) diabetes mellitus + exposure, 2) diabetes mellitus + sham exposure, 3) healthy rats + exposure, 4) healthy rats + sham exposure. Streptozotocin was given to produce diabetes mellitus.
Exposure duration: 4 x 30 min/day with 15 min intervals, for 30 days
|magnetic flux density||5 mT||-||measured||-||-|
Mechanical responses: Contraction of the aorta rings was significantly higher in non-diabetic rats (group 3, 4) than diabetic rats (group 1, 2). Within the diabetic groups, contraction was significantly lower in group 1. After submaximal contraction with phenylephrine, acetylcholine produced a significant relaxation in all aorta rings, which was significantly lower in diabetic groups (group 1, 2). Within the diabetic groups, the relaxation was significantly greater in the exposure group (1).
Membrane potential changes: Resting potentials were significantly higher in diabetic than non-diabetic groups. The pulsed electromagnetic field exposure did not induce significant effects on the membrane potential.
Diabetes reduced the relaxation of thoracic aorta rings and affected the membrane potentials. Treatment with pulsed electromagnetic fields improved the diabetes-induced impairments in the relaxation response of the rings.