ABSTRACT
The first Japan-Korea workshop on acupuncture and EBM was held on June 4, 2004 at Chiba in the 53rd annual scientific meeting of the JSAM. The purpose of this workshop was to exchange the experiences of clinical researches on acupuncture and moxibustion therapies, and to find out the issues and their solutions for developing the excellent clinical research to establish strong evidence. The final purpose was to develop aprotocol for the collaborative work between both countries.<BR>Drs. Kawakita (JSAM) and Jang (KAMS) chaired the workshop. Three speakers from Japan (Drs Takahashi, Nabeta, and Tsukayama) and three Korean speakers (Drs Seo, Lee and Moon) presented their data on the clinical researches of acupuncture, moxibustion and bee-venom injection. After their paper presentations, various issues were discussed on their research methodology for establishing more strong evidence of acupuncture.We got interesting new findings and understood various issues for conducting clinical researches especially RCT.<BR>Although we could not develop a protocol for the collaborative research in this workshop, it was very fruitful workshop as the first step for the future Japan-Korea collaborative clinical study. The most important product of this workshop was we could understand each other and we confirmed the necessity of the future collaborative clinical research on acupuncture.
ABSTRACT
By using extracellular single unit recording technique, locally suppressive effects of a single dose of ketamine on sub-cutaneous (s. c. ) bee venom-induced increase in firing of wide dynamic-range (WDR) neurons in spinal dorsal horn were investi-gated on urcthane-chloralose anesthetized cats. Injection of bee venom s.c. into the cutaneous receptive field (RF) resulted in asingle phase of prolonged, persistently increased firing of WDR neurons over background activity for more than 1 h. Local pre-treatment with ketamine (100 mM, 0. 1 m l) into the center of RF where bee venom was injected produced a dramatic suppressionof the increased neuronal firing by 60% (3.10± 0.42 spikes/s, n= 5) when compared with saline pre-treated group (7.61 ± 0.17spikes/ s. n = 5 ). Moreover, local post-treatment with the same dose of ketamine also produced a profound suppression of the in-creased neuronal activity by 81% (1.51±0.06 spikes/s, n=5) when compared with the saline post-treated group (7.76±0.15spikes s, n=5). However, s.c. administration with the same dose of ketamine into a symmetrical region on the bee venom un-treated contralateral hindpaw produced no affection on the increased firing of the WDR neurons, suggesting that the suppressiveaction of local ketamine was not the result of systemic effects. The present result suggests that ketamine may exert its localantinociceptive effects mainly through the peripheral NMDA receptors in addition to its partially potential blocking effects onsodium and voltage-sensitive calcium channels.
ABSTRACT
The present study was to investigate whether peripheral NMDA receptors were involved in the persistent nociceptioninduced by subcutaneous (s. C. ) bee venom injection in the conscious rat by using quatitative pain scoring methods, a.c. Bee venom injection into one hindpaw resulted in a persistent, monophasic nociceptive response characterized by continuously flinching.lifting and licking the injected paw for more than I h. The non-competitive. NMDA receptor channel blockers, ketamine and ME-801, were administered s.c. 5 or 20 min after bee venom. Local ketamine injection produced a suppression of flinching reflex by 20. 90±2.88% and 45.76±13.9%, while that of lifting/bcking time by 39. 53±10. 05% and 59.94±5.53%, at doses of 25mmol/L and 50 mmol/L respectively without any motor disturbance, Local MK-801 resulted in an inhibition of flinching reflexby 22.84±3.12% and 49.53±5.35%. While that of lifting/licking time by 17. 49±5.67%and 53.49±3. 87%. At doses of 10μmol/L and 100 ,μmol/L respectively also with no motor disturbance. However, s. C. Administration of ketamine and MK-801 inior region symmetrical to the bee venom injection site on the contralateral hindpaw produced no change in the nociceptive behaviors, suggesting that the analgesic actions of keramme and MK-8Ol were not the result of systemic effects. The present resultsuggests that peripheral NMDA receptors are involved in the production of persistent pain.