Mast Cell Degranulation and Adenosine Release:Acupoint Specificity for Effect of Electroacupuncture on Pituitrin‐Induced Acute Heart Bradycardia in Rabbits

Abstract

Acupuncture is a medical modality based on the theory of traditional Chinese medicine, and its effect is relatively dependent on acupoint specificity. However, there is little knowledge on acupoint specificity versus acupuncture outcomes because of the deficiency of rigorous investigation on this topic, which has impeded the growing legitimacy of acupuncture in the mainstream of medicine as an evidence-based therapy. Therefore, it is of utmost importance to clarify this critical issue. The present study aims to verify the phenomenon of acupoint specificity in acupuncture-induced cardiovascular regulation and explore the biological mechanism by measuring mast cells’ degranulation and adenosine release. This study was conducted to explore the specificity of acupoints in an acute bradycardia rabbit model. After electroacupuncture (EA) stimulation at PC6, PC control (con) 1, PC con 2, LU7, LI11, and nonacupoint, only the PC6 group showed a significant improvement in relative heart rate as compared to that of the model group. There was no significant difference between the relative heart rate of other EA groups and that of the model group. Historical results also showed that the ratio of degranulated mast cells in PC6 was significantly higher than other acupoints and control points. From the results of high-performance liquid chromatography (HPLC), a transient elevation of adenosine concentration during EA was only observed on acupoints and control points ( P < 0.05 ) along the pericardium meridian. The EA-induced adjustment on acute bradycardia exhibits a relative specificity of acupoints, which may be related to mast cell degranulation and adenosine release in local acupoint areas. Increased degranulation of mast cells and augmentation of adenosine release during EA may be the mechanisms for PC6 having significantly better acupuncture effects than other acupoints and nonacupoints.

Mast Cells and Acupuncture Analgesia

“…Moreover, He et al found that the concentration of substance P, a calcitonin gene related peptide, at the same acupoint, is different under normal, pathological, and acupuncture conditions [ 51 ]. Using high-performance liquid chromatography (HPLC) to measure the adenosine concentration at acupoints, Wang et al found significant differences before and after modeling and acupuncture [ 52 ]. These findings imply a dynamic variation of chemicals at the acupoints, manipulated by the inner environment or the external stimulation.…”

Effect of Acupoint Catgut Embedding for Abdominally Obese Female with Strong Appetite: Mixed Analysis of a Randomized Clinical Trial

“…26,27 Therefore, in related studies, non-acupoints were usually used as sham control to verify the specificity of acupoints. 28,29 The non-acupoint area parallel to the acupoint and meridians were usually selected as the contrast sites. Stimulating the non-acupoint sites generates definite effects, but not limited to the local nearby effects.…”

“…After the stimulation at acupoint, the Qi effect, degranulation of mast cells, adenosine release, and the regulation of brain network and target organ are also different. 27,29,30 Therefore, whether strong appetite or moderate appetite, the same acupoint stimulation plays the similar effect. This trial has several limitations.…”

Activation of Subcutaneous Mast Cells in Acupuncture Points Triggers Analgesia

“…There are three main ways of MC activation: immunogenic, neurogenic and physical activation [ 4 , 29 ]. Many studies have confirmed that MCs play a central role in the initiation mechanism of acupuncture analgesic via degranulation [ 17 , 30 , 31 , 32 , 33 ]. In acute adjuvant arthritis (AA) model rats, acupuncture can induce the degranulation of subcutaneous MCs in treated ST36 [ 30 , 32 ], which can be prevented by local pre-administration of cromolyn (CRO), a stabilizer of MCs ( Figure 5 ).…”

“…Besides manual acupuncture, electroacupuncture also can mediate Ado aggregation. In pituitrin-induced acute heart bradycardia rabbits, Ado accumulation occurs in Neiguan point (PC6) treated by 30-min electroacupuncture [ 33 ]. In ankle inflammatory or neuropathic pain model mice, activation of Ado A1 receptors in acupoint ST36 by 2-Chloro- N 6-cyclopentyladenosine (CCPA), a specific agonist of A1 receptors, has an anti-nociceptive effect [ 69 ].…”