Estudo dos mecanismos endógenos mobilizados pela eletroacupuntura no ponto e36 para a indução de efeito antinociceptivo em modelo orofacial em ratos.

Abstract

In the present study, it was investigated the capacity of electroacupuncture at the St36 acupoint in activate the endogenous pathways NO/cGMP/KATP, cannabinoids, GABA and noradrenaline, to obtain orofacial antinociception in rats. For this, it was used, as algesimetric model, a tail-flick test modification, described by Damour & Smith (1941) in which the termal stimulation is applied in the face, instead of the tail of the animal. Results demonstrated that acupuncture is able to activate the NO pathway, with the participation of neuronal and inductible NOsintase isoforms, since the intraperitoneal injection of both specific antagonists N-propil-L-arginine (1 and 2 mg/kg) and aminoguanidine (0.5, 1 and 2 mg/kg), respectivelly, were able to reverse the rat facial withdrawal threshold produced by acupuncture. That effect was not observed when a specific endothelial NOsintase antagonist, L-NIO, was used. Furthermore, measurement by colorimetry technique of nitrite, a NO metabolite, shows a significative growing (2-fold) in plasmatic concentration after electroacupunture stimulation. This increasing was more pronounced in cerebrospinal fluid (4-fold). The endocannabinoid pathway seems to be also involved in this orofacial antinociception, since that previous injection of the CB1 specific antagonist, AM 251, was capable in block this acupuncture effect, both when the intraperitoneal (1 and 2 mg/kg), as ICV (1 and 2 g) injection were used. Curiously, this effect was not obtained when intra-thecal injection was used to administrate AM251. MAPF (1 and 2 mg/kg), inhibitor of FAAH, enzyme that produce degradation of anandamide, and VDM 11 (5 and 10 mg/kg), inhibitor of anandamide reuptake, were capable to produce a growing in the acupuncture antinociception both in intensity and duration of effect. However, AM 630 (1 and 2 mg/kg), a CB2 specific antagonist, was not able to produce any modification in this analgesic effect produced by acupuncture in St36 acupoint. The GABAergic and noradrenergic systems seem not to be involved with the acupuncture orofacial antinociception since saclofen (20 mg/kg), a GABAB specific antagonist, guvacine (20, 40 and 80 mg/kg), inhibitor of GABA reuptake, and yoimbine (1, 2 and 4 mg/kg), a 2 specific antagonist did not provoke any modifications at no one tested doses. These data suggest the participation of NO/cGMP/KATP and endocannabinoid pathways in the acupuncture orofacial antinociception obtained by St36 acupoint, and that this effect seems to occur by structures by the supraspinal central nervous system.