Efeito antinociceptivo e mecanismos de ação da corrente interferencial na antinocicepção em modelo experimental de inflamação articular

Abstract

Introduction: Interferential current (IC) has been currently used for different clinical conditions, mainly for the purpose of analgesia. However, little is known about the mechanism of neurobiological action of this current. The objective of this study was to investigate the effect of IC on sensory and motor intensity in the hypernociception caused after induction of joint inflammation and if, systemically, the cholinergic, monoaminergic and nitric oxide receptors are involved in the mechanism of antinociceptive action of this current. Material and methods: A total of 96 Wistar rats were divided into experimental series (Control, Motor and Sensory) and pharmacological block series (Control, CI + Saline, CI + DMSO, CI + Reserpine, CI + CI + Atropine, CI + Haloperidol, CI + L-NNA, CI + ODQ, CI + Glibenclamide). Electrical stimulation was applied 24 hours after the induction of inflammation and in the reserpine group with 48h due to its mechanism of action. Behavioral tests for sensitivity and motor performance were performed before induction, 24 hours after induction of inflammation and after IC application. Pharmacological blockade was achieved by intraperitoneal injection applied prior to treatment according to the time of action and dose of each drug. Values of p <0.05 were considered significant. Results: In the behavioral series, there was an increase in the cutaneous sensory threshold (p = 0.03) in the group treated with motor intensity, and an increase in the thermal latency in the groups treated with sensory and motor intensities (p <0.009), the motor group presented greater effect size in the mechanical sensitivity (d = 1.42). In contrast, high intensity promoted a decrease in motor performance (p = 0.03) compared to pre-treatment. In the series that evaluated the possible mechanisms of action in the reserpine series, it was identified that amine depletion prevented the increase of the cutaneous sensory threshold in the IC + Reserpine group differently from the IC + Saline group in which there was antinociception (p = 0.01). Of the monoamines investigated, there was an impediment in the effect of the current on the sensory threshold in the CI + Yohimbine and CI + Atropine groups, since there was no difference between the pre and post treatment groups differently from CI + Salina, CI + Prazosin and CI + Haloperidol (p < 05). Inhibition of nitric oxide synthase (NOS) in the CI + L-NNA group prevented IC-promoted antinociception and in the intracellular cascade of this pathway both guanylate cyclase and dependent K-channels were found of ATP also participate in their antihyperalgesic mechanism because they do not increase the mechanical threshold after IC treatment. All groups treated with IC plus vehicle or antagonists had a reduction of the distance covered (p <0.03) less control and CI + yohimbine groups. Conclusion: Based on the present study, we can conclude that the interferential current in motor intensity is more effective for the reduction of antinociception and that this effect involves mechanisms of action of the alpha-2 receptors, muscarinic cholinergic and is related to the nitric oxide pathway.