Electroacupuncture at LI11 promotes jejunal motility via the parasympathetic pathway

Abstract

BackgroundGastrointestinal motility disorder has been demonstrated to be regulated by acupuncture treatment. The mechanisms underlying the effects of acupuncture stimulation of abdominal and lower limb acupoints on gastrointestinal motility have been thoroughly studied; however, the physiology underlying the effects of acupuncture on the forelimbs to mediate gastrointestinal motility requires further exploration. The aim of this study was to determine whether electroacupuncture (EA) at LI11 promotes jejunal motility, whether the parasympathetic pathway participates in this effect, and if so, which somatic afferent nerve fibres are involved.MethodsA manometric balloon was used to observe jejunal motility. The effects and mechanisms of EA at LI11 were explored in male Sprague-Dawley rats with or without drug administration (propranolol, clenbuterol, acetylcholine, and atropine) and with or without vagotomy. Three types of male mice (β1β2 receptor-knockout [β1β2 −/−] mice, M2M3 receptor-knockout [M2M3 −/−] mice and wild-type [WT] mice) were also studied by using different EA intensities (1, 2, 4, 6, and 8 mA). A total of 72 rats and 56 mice were included in the study.ResultsEA at LI11 increased the contractile amplitude of jejunal motility in the majority of both rats and mice. However, EA at LI11 did not enhance jejunal motility in rats administered atropine, rats that underwent vagotomy, and M2M3 −‍‍/− mice (at all intensities). In WT mice, EA at LI11 significantly increased jejunal motility at all intensities except 1 mA, and a plateau was reached at intensities greater than 4 mA.ConclusionOur results suggest that EA at LI11 promotes jejunal motility primarily by exciting the parasympathetic pathway, and that Aδ-fibres and C-fibres may play important roles in the process.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-017-1826-9) contains supplementary material, which is available to authorized users.

Neuromechanism of acupuncture regulating gastrointestinal motility

“…The role of the somatoautonomic reflex, which was demonstrated by Sato and his colleagues in the 1960s[ 34 , 35 ], is now considered the neurological basis of acupuncture in GI motility modulation[ 36 , 37 ], and this modulation exerts a regional-specific effect[ 38 , 39 ] (Figure 1 ). Stimulating acupoints in the abdominal area inhibits gastric, duodenal, and jejunal motility by increasing sympathetic efferent fiber activity, and stimulating acupoints in the limb, which, in contrast, facilitates the above-mentioned gut motility by exciting vagal efferent fiber activity[ 18 , 40 - 43 ]. The effect of acupuncture on GI motility could be attenuated by vagotomy or sympathectomy[ 16 , 44 - 46 ].…”

Electroacupuncture at ST36 modulates gastric motility via vagovagal and sympathetic reflexes in rats

“…As stated, EA regulates gastrointestinal motility via the vagus and sympathetic nerves. Studies have shown that injection of the M receptor blocker atropine can inhibit the gastric motility-promoting effect of EA at LI11 (Quchi)[25], and the injection of the beta blocker propranolol can abrogate the inhibition of jejunal motility[26]. However, due to a poor specificity of the blockers, the specific receptor subtype(s) through which these effects are mediated is not clearly known.…”

Electroacupuncture Stimulation Regulates Adipose Lipolysis via Catecholamine Signaling Mediated by NLRP3 Suppression in Obese Rats

“…Electroacupuncture was performed at the forelimb LI11 (Quchi) acupoint by inserting a pair of stainless-steel acupuncture needles (diameter: 0.3 mm) up to 3 mm in depth at each site. LI11 is located midway between the lateral end of the transverse cubital crease and the lateral humeral epicondyle ( 17 ). The needles were connected to Han’s electroacupuncture instrument (LH402A; Beijing Huawei Technologies Co. Ltd).…”