Hu Xuanming, Yuan Mengqian, Yin Yin, Wang Yidan, Li Yuqin, Zhang Na, Sun Xueyi, Yu Zhi, Xu Bin
Key Laboratory of Integrated Acupuncture and Drugs Constructed, Nanjing University of Chinese Medicine, Ministry of Education, Nanjing, 210023, China.
BMC Complement Altern Med. 2017 Jun 21;17(1):329. doi: 10.1186/s12906-017-1826-9.
Gastrointestinal 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.
A 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 (ββ receptor-knockout [ββ] mice, MM receptor-knockout [MM] 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.
EA 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 MM 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.
Our 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.
胃肠动力障碍已被证明可通过针刺治疗得到调节。针刺刺激腹部和下肢穴位对胃肠动力影响的机制已得到深入研究;然而,针刺前肢对胃肠动力影响的生理学机制仍需进一步探索。本研究的目的是确定针刺手三里穴是否能促进空肠蠕动,副交感神经通路是否参与此效应,若参与,涉及哪些躯体传入神经纤维。
使用测压气囊观察空肠蠕动。在雄性Sprague-Dawley大鼠中,通过给药(普萘洛尔、克伦特罗、乙酰胆碱和阿托品)或切断迷走神经,探讨针刺手三里穴的效应及其机制。还使用不同强度(1、2、4、6和8毫安)的电针刺激,对三种雄性小鼠(ββ受体敲除[ββ]小鼠、MM受体敲除[MM]小鼠和野生型[WT]小鼠)进行了研究。本研究共纳入72只大鼠和56只小鼠。
针刺手三里穴可增加大多数大鼠和小鼠空肠收缩幅度。然而,针刺手三里穴对给予阿托品的大鼠、接受迷走神经切断术的大鼠以及MM小鼠(所有强度)的空肠蠕动没有增强作用。在WT小鼠中,除1毫安外,针刺手三里穴在所有强度下均显著增加空肠蠕动,且在强度大于4毫安时达到平台期。
我们的结果表明,针刺手三里穴主要通过兴奋副交感神经通路促进空肠蠕动,并且Aδ纤维和C纤维可能在此过程中发挥重要作用。