Philip A.M. Rogers MRCVS

AP and Neurology


Bing_Z; Cesselin F; Bourgoin S; Clot AM; Hamon M; Le Bars D (1991) AP-like stimulation induces a heterosegmental release of Met-Enk-like material in the rat spinal cord. Pain Oct 47(1):71-77. INSERM U. 161, Paris, France. Either the lumbar or the cervicotrigeminal area was perfused with artificial CSF (0.1 ml/min) in halothane-anaesthetized rats in order to study the effects induced by AP on the activity of enkephalinergic neurons in the spinal cord. Met-Enk-like material (MELM) was measured in 0.5 ml fractions of the perfusates. The effects of manual AP performed by a traditional Chinese acupuncturist at ST36 on the right hind limb were compared to the effects induced by AP applied at a non-AP point near ST36. The manipulation of needles either at the ST36 point or at the non-AP point had no effect on the release of MELM from the lumbar area but significantly increased the release from the cervicotrigeminal zone. It is concluded that manual AP triggers a heterosegmental activation of enkephalinergic neurones within the spinal cord and that this effect is non-specific in terms of the location of the stimulated point.

Bing_Z; Villanueva L; Le Bars D (1990) AP and diffuse noxious inhibitory controls: naloxone-reversible depression of activities of trigeminal convergent neurons. Neuroscience 37(3):809-818. INSERM, Unité de Recherches de Physiopharmacologie du Système Nerveux, Paris, France. Recordings were made from convergent neurons in trigeminal nucleus caudalis of the rat. These neurons were activated by both innocuous and noxious mechanical stimuli applied to their excitatory receptive fields on the ipsilateral part of the muzzle. Percutaneous application of suprathreshold, 2 ms square-wave electrostimuli to the centre of the excitatory field evoked responses to A- and C-fibres. The effects on these responses of manual AP, given by a traditional Chinese acupuncturist at ST36 on the right hindlimb were compared with the effects induced by AP applied at a non-AP point, near ST36. Also, the effects of AP were compared with the inhibitory effects evoked by noxious thermal stimulation of the left hindlimb on the responses of the same neurons. Earlier, our group has termed the latter type of inhibition "diffuse noxious inhibition". AP, either applied at ST36 or at a non-AP point and noxious thermal stimulation induced similar strong inhibitory effects on the C-fibre-evoked responses of trigeminal convergent neurons (77.9+4.4%; 72.5+4.6% and 78.5+3.6% inhibition, respectively) and these inhibitions were followed by long-lasting aftereffects. Also, both the AP- and noxious thermal stimulation-evoked inhibitions were significantly reduced by systemic naloxone (0.4 mg/kg, iv). Since the antinociceptive effects elicited by AP (i) had a similar magnitude and time-course to those evoked by noxious thermal stimulation, (ii) exhibited a lack of topographical specificity and (iii) involved an opioidergic link, we would suggest that, at least in our experimental conditions, AP manoeuvres trigger the neuronal mechanisms involved in diffuse noxious inhibitory controls.

Bing_Z; Villanueva L; Le Bars D (1991) AP-evoked responses of subnucleus reticularis dorsalis neurons in the rat medulla. Neuroscience 44(3):693-703. INSERM U. 161, France. Recordings were made from neurons in subnucleus reticularis dorsalis of rats. 2 populations of neurons were distinguished: those with total nociceptive convergence which were driven by activating A delta- and C-fibres from any part of the body and those with partial nociceptive convergence which were driven by activating A delta-fibres from any part of the body or C-fibres from some, mainly contralateral, regions. The effects on subnucleus reticularis dorsalis neurons of manual AP, performed by a traditional Chinese acupuncturist at GV26, LI10, GV01, and ST36, and at a non-AP point near ST36, were studied. AP stimulation for 30 s at the AP points or the non-AP point strongly excited all the total nociceptive convergence neurons tested; these neurons responded with a discharge of rapid onset which was often followed by after-discharges lasting for circa 30-60 s. Most but not all of the partial nociceptive convergence neurons responded to 30 s of AP stimulation at the AP points or the non-AP point. This was especially the case when the stimulus was applied to contralateral or midline parts of the body. The potency of AP as a means of activating neurons in the subnucleus reticularis dorsalis varied significantly with the area of the body being stimulated such that: contralateral > midline > ipsilateral areas. The levels of induced activity were of similar magnitude to those evoked by noxious mechanical stimuli applied under identical experimental conditions. No differences were found between the capacities to activate subnucleus reticularis dorsalis neurons of ST36 and the adjacent non-AP point, no matter whether these were stimulated ipsi- or contra- laterally; this suggests a lack of topographical specificity in the activation of these neurons. Since subnucleus reticularis dorsalis neurons are activated exclusively or preferentially by noxious inputs, it is concluded that the signals elicited by manual AP travel through pathways responsible for the transmission of nociceptive information. Since AP, a manoeuvre which is known to elicit widespread extrasegmental antinociceptive effects, activates subnucleus reticularis dorsalis neurons which, anatomically, send dense projections to the dorsal horn at all levels of the spinal cord, we would suggest that this structure may be involved not only in signalling pain but also in modulating pain by means of spino-reticulo-spinal feed-back mechanisms.

Cai_B; Huang X; Wang G; Mo W (1994) Potentiation of EAP-analgesia on visceral pain by metoclopramide and its mechanism. Chen Tzu Yen Chiu - AP Research 19(1):66-70, 74. Dept of Neurobiology, Shanghai Med Univ, PRC. This was a study of the effect of metoclopramide (MCP) on EAP analgesia (EAA) and its mechanism on a rabbit visceral pain model. MCP 8mg/kg iv enhanced EAA and prolonged the analgesic duration. The potentiation effect was attenuated by icv apomorphine (a mixed D1/D2 agonist). The duration of EAA was shortened by icv SKF38393 (a selective D1 agonist) or LY171555 (a selective D2 agonist). Using HPLC-ECD, the HVA level in CSF significantly increased at 20 min after EAP or MCP 8mg/kg iv.

Cao_Q; Liu J; Han Z; Wang H (1992) Influence of AP on the discharge of PHA neurons in the rabbit. Chen Tzu Yen Chiu 17(1):21-25. Inst of AP and Moxibustion, China Acad of TCM, Beijing, PRC. This paper deals with whether the posterior hypothalamus area (PHA) can receive signals from EAP at PC06, and whether a relative specificity exists between AP points or between AP points and non-AP points. Neuronal activity was recorded extracellularly to analyze the influence of EAP at different AP points and non-AP point on the discharge of PHA neurons.

Chen_SZ; Han JS (1994) High frequency EAP-induced changes of IP3 level in rat brain and spinal cord. CMJ (UK) Jun 107(6):440-3. Neuroscience Research Centre, Beijing Med Univ, PRC. In this study, the radioreceptor binding method was used to determine the changes of IP3 level in the brain and dorsal spinal cord of rats with high frequency (100 Hz) EAP analgesia (EAA) and of rats tolerant to EAP. Control levels of IP3 in rat brain (less cortex and cerebellum) and dorsal spinal cord were 6.3+0.78 and 3.4+0.60 pmol/mg protein, respectively. IP3 in brain increased gradually within 45 min after EAA. Meanwhile, IP3 level in the dorsal spinal cord decreased significantly 15 min, 30 min after EAA and recovered to control level 45 min after EAA. Brain IP3 level markedly increased in EAP-tolerant rats a spinal cord IP3 level also increased dramatically within 30 min, but decreased rapidly to control level 45 min after EAA. The IP3 level in brain and spinal cord of EAP-tolerant rats was much higher than that in EAA-rats.

Chen_XH; Geller EB; Adler MW (1996) EAP at traditional peripheral AP sites produces brain opioid-receptor-mediated antinociception in rats. J Pharmacol Exp Ther May 277(2):654-60. Dept of Pharmacol, Temple Univ Sch of Med Philadelphia, Pennsylvania, USA. Previous studies in rats measuring latency to tail flick with radiant heat have shown that the antinociceptive effect induced by EAP at different frequencies at traditional AP sites is mediated via different opioid receptors in the spinal cord. The present study was designed to observe: 1. whether EAP at such sites could produce antinociceptive effects in the cold water tail-flick (CWT) test; 2. whether the antinociceptive effects could be blocked by sc injection of the opioid receptor antagonist naloxone and (3) whether icv injection of selective antagonists for mu (cyclic D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2, CTAP), delta (naltrindole) or kappa (nor-binaltorphimine) opioid receptors would block the antinociceptive effect produced by EAP stimulation. Sprague-Dawley rats were stimulated by EAP at frequencies of 2, 30 or 100 Hz by needles at ST36 and SP06 for 30 min. Antinociception was assayed in the CWT. As compared with the placebo group, a significant frequency-related increase in threshold in the CWT occurred in all EAP-groups, and the antinociceptive effect lasted circa 30 min poststimulation. Naloxone sc antagonized the antinociceptive effect induced by EAP at 2 Hz, 30 Hz or 100 Hz. Either CTAP or naltrindole icv almost eliminated the antinociceptive effect induced by EAP at 2 Hz or 30 Hz, but was less effective in blocking antinociception induced by EAP at 100 Hz; nor-binaltorphimine (icv) greatly reduced antinociception induced by EAP at 30 Hz or 100 Hz, but not at 2 Hz. Antinociception induced by EAP at 2 Hz is mediated by both mu and delta opioid receptors; that induced by EAP at 100 Hz is mediated primarily by the kappa receptor. The antinociception induced by EAP at 30 Hz is mediated by all 3 opioid receptor types. Thus, as measured by the CWT, the antinociceptive effect induced by peripheral electrostimulation involves opioid receptors in the rat brain.

Chen_XH; Han JS; Huang LT (1994) CCK receptor antagonist L-365,260 potentiated EAP-analgesia in Wistar rats but not in audiogenic epileptic rats. CMJ (UK) Feb 107(2):113-118. Dept of Physiology, Beijing Med Univ, PRC. CCK octapeptide (CCK-8) is a neuropeptide with potent anti-opioid activity. Morphine analgesia is mediated by CCK-B receptor in CNS. Nanogram doses of CCK-8, administered to the CNS, totally abolished morphine analgesia in rats. In the present study CCK-B antagonist L-365,260 was injected icv to Wistar rats to see its effect on the analgesic effect induced by EAP. A marked potentiation of EAA was observed. The degree of potentiation depended on the frequency of EAP used, with a rank order of 100 Hz > 15 Hz = 2-15 Hz >> 2 Hz. In a rat-strain with acoustically evoked epileptic seizure (P77PMC rats), an very powerful analgesic effect was produced in response to 100 Hz EAP, which was similar to that in Wistar rats pre-treated with L-365,260. However, L-365,260 was not effective in potentiating EAA in P77PMC rats. Conclusions: 1. high frequency EAP is more likely to increase the release of CCK-8 in CNS as compared to low frequency EAP; 2.P77PMC rats may have a functional defect of CCK neurons in the CNS, either a low CCK level, or a reduced rate of release of CCK-8.

Chen_Y; Wang Y; Yin Q (1991) [The role of paraventricular nucleus of hypothalamus in APA in rats]. Chen Tzu Yen Chiu 16(1):32-38. Dept of Physiol, Suzhou Med Coll. Recent evidence has indicated that vasopressin (VP) can increase the pain threshold. It is not clear whether the hypothalamic paraventricular nucleus (PVN), one of the main VP-secreting nuclei in the brain, is involved in APA. The present study was designed to examine the role of PVN in APA, using Wistar rats. The tail-stimulation vocalization test was used to measure pain threshold. GV26 and CV24 were selected for EAP. Electrostimulation of PVN significantly increased the pain threshold and enhanced the effect of APA. On the contrary, electrolytic lesion of PVN clearly decreased the effect of APA, which was restored by icv injection of 300 ng of arginine VP. Pretreatment with AVP-antiserum (ICV) attenuated the effect of APA. PVN plays an important role in pain modulation and in the effect of APA. This role may be mediated by VP-containing neurons in PVN.

Chen_Za1; Yan Y; Xu W; Shi T (1990) [Relationship between the precruciate cortex and the ventral lateral posterior nucleus of the thalamus in APA]. Chen Tzu Yen Chiu 15(1):61-65. Inst of AP and Moxibustion, China Acad of TCM, Beijing. The present study was designed to investigate the relationship between the precruciate cortex (PreCtx) and the ventral lateral posterior nucleus (VPL) of the thalamus in the mechanisms of APA. Neuronal responses in the nucleus VPL to noxious electrostimulation of the superficial peroneal nerve were recorded extracellularly. Lidocaine was topically applied at PreCtx 20 min after EAP was given at ST36 and GB30 for 5 min. Nociceptive responses were recorded immediately after cessation of EAP and consecutively recorded at 2 min intervals. Similar procedures were made in the control group, in which 0.9% NaCl was topically applied at PreCtx. It was found that topical application of lidocaine at PreCtx did not influence the nociceptive responses of VPL neurons. After topical application of lidocaine at PreCtx, the nociceptive responses were obviously inhibited 0, 4, 6, 10, and 12 h after cessation of EAP. In the saline control group the remarkable inhibitory effect of EAP was observed 0-8 h after ceasing EAP. The inhibitory effect of EAP in the test group was weaker than that in the control group. However, the difference was not statistically significant. PreCtx may participate in the corticofugal modulation of EAP effects in the nucleus VPL only to small extent.

Chen_Za2; Shi H; Wu G; Zheng X; Xu W (1995) [Influence of SmI lesion on AP-induced analgesia in thalamic Pf neurons and effects of iontophoretic ACh on their nociceptive responses]. Chen Tzu Yen Chiu 20(1):15-19. Inst of AP and Moxibustion, China Acad of TCM, Beijing. This study aimed to investigate the role of ACh in SmI emanating descending modulation of thalamic Pf neurons in APA. Multi-micropipettes were used for both extracellularly recording responses of thalamic Pf neurons to noxious stimulation of the plantar area and drug application in rats. Results: 1. Lesion of SmI obviously attenuated the inhibitory effect of EAP applied at ST36 and GB30 on nociceptive responses in Pf neurons; 2. After lesion of SmI iontophoretic application of ACh markedly suppressed the nociceptive responses of Pf neurons, which was significantly different from the effect of iontophoretic NaCl (as the control) showing no influence on them; 3. The inhibition induced by iontophoretic ACh applied in the rats with lesion of SmI was similar to that produced by EAP applied in those with SmI intact. EAP activated SmI to release ACh to exert descending modulation, in which ACh was involved in SmI originating descending regulation of Pf neurons in APA.

Chen_Zb1; Chen P (1991) [Effects of morphine and EAP on the time-lock and not-time-lock responses of cortical unit discharges evoked by nociceptive stimulation in cats]. Chen Tzu Yen Chiu 16(2):95-99. Dept of Physiol, Sun Yat-Sen Univ of Med Science, Guangzhou, PRC. In order to study the effects of morphine and EAP(EA) on non-time-lock response (N-TLR) and time-lock response (TLR) of nociceptive unit discharges, N-TLR was shown by interspike interval mean function (ISIMF) and TLR by normalized cross-covariance function (NCCVF) reflecting the relationship between stimulation and response. The N-TLR elicited by the noxious stimulation appeared as a decrease of ISIMF, which was depressed obviously by EA and morphine, but the inhibitory effect of EA was more rapid than morphine; both EA and morphine inhibited mainly the late peak of the NCCVF elicited by the noxious stimulation, but inhibitory effect of EA developed more rapidly and recovered more quickly than that of morphine. The inhibitory effect of EA on the early peak was very little. P-ED elicited by the noxious stimulation is inhibited by both EA and morphine, but the degree and the speed of inhibition were different. [Question by Rogers: Are cats not unpredictable responders to morphine ?].

Cui_R; Zhao F; Ma C; Tian Y; Cai H; Zhu L (1992) [Influence of 5,7-dihydroxytryptamine on EAP analgesia and Substance-P level in the CNS of arthralgic rats]. Chen Tzu Yen Chiu 17(3):183-185. Inst of AP and Moxibustion, China Acad of TCM, Beijing. The relation between EAP analgesia and Substance-P (SP) level in the brain stem (BS) and lumbar spinal cord (LSC) of arthralgic rats was investigated. The rats were assigned to 3 groups: 1=EAP + 5,7-7DHT (5,7-dihydroxytryptamine); 2=EAP + V (vehicle); 3=5,7-DHT. To induce joint-pain, Freund's adjuvant was injected into joints of all animals 7 d after icv injection of 5,7-DHT or vehicle. The SP level in the BS and LSC was determined by RIA. Compared to group 3, EAP prolonged tail flick latency by 39.6% in group 2, but not in group 1. The SP level in LSC of group 2 (179.1+11.5 pmol/g) was higher than that in group 1 (135.9+9.3pmol/g) and group 3 (125.8+10.0 pmol/g). EAP and arthralgia both activated the descending 5-HT-ergic inhibitory system, which inhibited the release of SP in LSC. Electro-APA was attenuated when the 5-HT-ergic system was destroyed by 5,7-DHT; the SP level in LSC was lowered due to its decreased release in EAP and arthralgia.

Cui_R; Ma C; Wang X; Tian Y (1990) [The influence of P-chlorophenylalanine (PCPA) on the analgesia of EAP and the level of SP in CNS of rats]. Chen Tzu Yen Chiu 15(2):109-111. Inst of AP and Moxibustion, China Acad of TCM, Beijing. PCPA 250 mg/kg IP, was given to a group of rats. 72 hrs later the EAP analgesia was tested and Substance-P (SP) in the brain stem and the lumbar spinal of the rats was determined by RIA. After PCPA injecting the EAP no longer caused analgesia but lowered the pain threshold. Meanwhile the level of SP in the brain stem and lumbar spinal did not increased but much lowered than the group of vehicle injection combined with EAP. By PCPA depleting the 5-HT in CNS and abating the descending inhibition activated by 5-HT, EAP no longer causes analgesia but promotes the SP transmitted release. Transmission of SP in the lower brain stem and spinal cord was regulated by descending inhibition. Analgesia of EAP activates the 5-HT-ergic descending inhibition and decreases the nociceptive transmission of SP partly.

Cui_Y; Chen G; Zhang Q; Jiang J; Wu G; Xu S (1990) [Effects of promethazine on APA]. Chen Tzu Yen Chiu 15(2):123-125, 122. Dept of Endocrinology, First Affiliated Hospital of Nanjing Med Coll. Promethazine, a histaminergic H1-receptor antagonist, was often used as an adjuvant drug before and during APA in clinics, but its effects on APA were not known clearly. By using K-iontophoretic dolorimetry and stimulating unilateral LI04 and TH05 with EAP in 42 rabbits, we found that Promethazine in small dosages (0.5 mg/kg, 1 mg/kg) decreased the pain threshold, and in relatively large dosages (2 mg/kg, 4 mg/kg) raised the pain threshold. At dosages of 1 or 2 mg/kg, promethazine attenuated the analgesic effect of EAP-analgesia. Promethazine should be used carefully in APA.

Dai_JL1; Xu SF (1991) The attenuation effect of chlorpromazine on EAP-analgesia: involvement of dopamine system. AETRIJ 16(3-4):101-109. Dept of Neurobiol, Shanghai Med Univ, PRC. The effect of chlorpromazine (CPZ) (0.1 or 0.5 mg/kg, iv) on EAP-analgesia (EAA) was examined by using potassium dolorimetry in rabbits. CPZ itself induced hyperanalgesia, whereas it attenuated EAA in terms of maximal increase of pain threshold as well as EAA after-effect. Thus, CPZ is not a good candidate for enhancing EAA in clinics. Monoamines and their metabolites in CSF of the rabbits were detected by HPLC coupled to electrochemical detector (HPLC-ECD) method. CPZ enhanced DOPAC and HVA levels in CSF in both the presence and absence of EAP. CPZ attenuated EAA with elevations of DOPAC and HVA level in CSF. There was a positive correlation between the increases of DOPAC and HVA levels in CSF and attenuation effect of CPZ on EAA. Activation of the dopamine system enhances EAP-analgesia.

Dai_JL2; Xu SF (1993) Chlorpromazine attenuated EAP-analgesia in conscious rabbits. Chung Kuo Yao Li Hsueh Pao Sep 14(5):388-392. Dept of Neurobiology, Sch of Basic Med Sci, Shanghai Med Univ, PRC. By measuring the defense behaviour in response to the noxious stimulation induced by K iontophoresis on ear-lobe skin of conscious rabbit, chlorpromazine (CPZ) (0.5 mg/kg iv) induced hyperalgesia, whereas it significantly attenuated the efficacy of EAA. Monoamines and their metabolites in CSF were measured by high pressure liquid chromatography with electrochemical detector (HPLC-ECD) while the attenuation effect of CPZ on EAA was observed. CPZ markedly enhanced 3,4-dihydroxyphenylacetic acid (DOPAC).

Dan'ko-SG; Bkhattachariia-N; Sharma-KN (1993) [Polyelectro-neurographic study of the dynamics of brain processes during AP in people with chronic pain syndrome]. Fiziol Cheloveka Mar-Apr 19(2):20-28.

Eriksson_SV; Lundeberg T; Lundeberg S (1991) Interaction of diazepam and naloxone on AP induced pain relief. AJCM 19(1):1-7. Dept of Med, Danderyds Hospital, Stockholm, Sweden. We have studied if 2 Hz EAP alleviates chronic nociceptive pain and if so whether the alleviation was related to the release of endogenous opioids. 32 patients suffering from osteoarthritis were subjected to EAP, with or without pretreatment with naloxone or diazepam. The effect of the different experimental procedures was assessed using scales for the intensity (sensory component) and unpleasantness (affective component) of pain. EAP induced a significant alleviation of pain. This alleviation was more significant on the affective scales (p <.01) than on the sensory scales (p <.05). After pretreatment with diazepam or naloxone, the subsequent pain alleviating effect was reduced. APA may partly be mediated through endogenous opioids which are affected by pretreatment with diazepam or naloxone.

Fan_T; Li J; Kong T (1993) [Relationship between APA and neurotransmitters in nucleus raphe magnus]. Chen Tzu Yen Chiu 18(3):168-171. Dept of Anatomy, Henan Med Univ, Zhengzhou. Nucleus Raphe Magnus (NRM) is a complex cell group. 5-HT, SP and ENK neurons in the NRM were identified by immunocytochemistry method. The afferent fibres containing 5-HT, SP, M-ENK, L-ENK, B-EP and SRIF were observed in NRM, the efferent fibres containing 5-HT, SP, ENK and TRH from NRM to spinal cord were studied. 2 neurotransmitters (such as 5-HT with SP, ENK or TRH) were found in same neuron, fibre or vesicle. The neurons and axodendritic synapses of the NRM were analyzed during EAP (EA). The NRM increased their synaptic releases and the neurons were in active functional state during EA of ST36. Studies show that NRM is one of important positions in EA analgesia.

Fang_J (1994) [The influence of AP at ST36 on cyclic nucleotide levels of plasma, different brain regions and spleen in rats]. Chen Tzu Yen Chiu 19(1):42-45. Nuclear medicine Lab, Shanghai Coll of TCM. We observed cyclic nucleotide level of plasma, brain and Spleen tissues when APA was produced by AP at ST36. The restrained group without AP was as blank control and AP at LV03 as AP control. We found that after AP at ST36 the level of cyclic nucleotide in plasma was increased significantly (p <.05) and the cAMP level of spleen had a tendency of enhancement, but the level of cAMP in the cortex had a tendency of decrease. The level of cAMP, cGMP and its ratio cAMP/cGMP was different in cortex and spinal cord between groups given AP at ST36 or LV03. AP at ST36 and LV03 induced different changes of level of cAMP and cGMP.

Fang_JQ; Liu YL; Mo XM (1994) [Clinical and experimental studies on analgesic effects of ipsilateral and contralateral stimulations with EAP]. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih Oct 14(10):579-582. Zhejiang Coll, TCM, Hangzhou. 65 cases of painful diseases were treated with EAP to compare the analgesic effect of contralateral stimulation (CS) and ipsilateral stimulation (IS). IS and CS gave similar degrees of pain-relief, but CS was better in improving motor impairment. The pain threshold of rats was tested and the neuronal activity in the D-PAG was recorded. Neither IS nor CS increased the pain threshold in the unilateral D-PAG lesioned rats, but excited neuronal discharge was recorded in the unilateral D-PAG by stimulating ST36 at each side. IS and CS may share the same high level afferent pathway in APA in CNS.

Fang_ZR; Li YH (1993) [The observation on analgesic effect of moxibustion in rats]. Chen Tzu Yen Chiu 18(4):296-269. Inst of AP & Moxibustion, China Acad of TCM, Beijing. Radiant heat exposure on BL32 was taken as radiant heat moxibustion (RHM). When temperature of surface of point was modulated within the range of 38-39 and 43-44oC, the latency of tail flick threshold (LTH) in rats was increased by 17.8+2.1% and 22.2+2.5% after 5 min. and by 16.1+2.9%, 22.1+3.4% and 21.9+3.2% (50-52oC) after 10 min. respectively. LTH was increased by 19.8+3.1% after 10 min. with AP plus moxibustion. The change of latency after RHM in every group and AP with moxibustion group was significant (p <.05). There was no difference of analgesic effect among all groups (p >.05). The APA effect of RHM on BL32 was more powerful than ST36 and BL67 (p <.05).

Fedoseeva_OV; Kalyuzhnyi LV; Sudakov KV (1990) New peptide mechanism of EAP-analgesia using Earpoints: role of angiotensin II. AETRIJ 15(1):1-8. PK Anokhin Inst of Normal Physiol, USSR Acad of Med Sciences, Moscow. Ear-EAP stimulation at frequencies of 15 and 100 Hz induced analgesia in rabbits, expressed by decrease amplitude of cortical SEPs in response to tooth pulp electrostimulation. Saralasin injection icv abolished or blocked the effect of Ear-EAP at 100 Hz, but not at 15 Hz. Naloxone injection iv abolished the effect of Ear-EAP stimulation at 15 Hz but not at 100 Hz. Methysergide or D,L-p-CPA injection diminished but did not entirely block the effect of Ear-EAP stimulation at 100 Hz. The neuropeptide angiotensin II may be a antinociceptive factor in dental peptide analgesic mechanisms induced by Ear-EAP stimulation at 100 Hz.