It has been reported by Stein et al. that the immune system and peripheral opioid receptors are involved in the control of pain accompanying inflammation. Electroacupuncture (EA) is used to relieve various kinds of pain. However, little is known about the effect of electroacupuncture analgesia (EAA) during hyperalgesia elicited by inflammation. The aim of the present study was to compare (1) the individual variation of EAA, (2) the durability of EAA, and (3) the effect of naloxone on EAA between normal rats and rats subjected to acute inflammatory pain. Carrageenan was subcutaneously administered by intraplantar (i.pl.) injection of the left hind paw to induce a nociceptive response. Nociceptive thresholds were measured using the paw pressure threshold (PPT). Rats received EA at 3 Hz in the left anterior tibial muscles for 1 hour after carrageenan injection. Naloxone was administered by intraperitoneal (i.p.) or i.pl. injection just before EA. EAA was elicited in 15 of 29 normal rats. These rats were divided into responders and non-responders. EAA in the responder group was almost completely antagonized by i.p. injection of naloxone. In contrast, in all the rats with carrageenan-induced inflammation, EAA was elicited, lasted for at least 24 hours after carrageenan injection, and was dose-dependently antagonized by i.pl. injection, but not significantly by i.p. injection of naloxone. It seems likely that the EAA in the rats with carrageenan-induced inflammation differs from that in normal rats, and these findings suggest that peripheral opioid receptors are involved in EAA during inflammatory conditions.
Effects of conditioning peripheral nerve stimulation with different types of stimulating electrodes on pain thresholds in various deep tissues were measured in human subjects. Cone-shaped metal (phi 13 mm), rubber (phi 13 mm), and large soft surface electrodes (50 x 150 mm) were used for transcutaneous electrical nerve stimulation (TENS), and insulated and non-insulated acupuncture needles (diameter: 240 microns) were used for electroacupuncture (EA). Two pairs of electrodes were placed around the point of deep pain measurement. Symmetrical positive and negative square pulses (0.1 msec at 100 Hz) of just below the pain tolerance intensity were used for both TENS and EA. Deep pain thresholds were measured at the center of the thigh with a pulse algometer and insulated needle electrodes. Pain thresholds of deep tissues were in the order periosteum < fascia < skin (including subcutaneous tissues) < muscle. TENS with surface electrodes significantly increased pain thresholds of skin and fascia but not those of muscle or periosteum. The shape, material and size of the surface electrodes hardly affected the degree of analgesic effect, except in the fascia by large soft electrodes. In contrast, EA with non-insulated needles induced a greater increase in pain threshold in skin, fascia and muscle, although statistically significant results were obtained in only the first two tissues. EA with insulated needle electrodes was the only technique with which we obtained a significant increase in pain threshold in muscle and periosteum. These results suggest that the choice of electrode and stimulus parameters is important for the production of sufficient analgesic effects in different somatic tissues and that insulated needle electrodes are useful for pain relief in deeper tissues such as muscle and periosteum.
Electroacupuncture (EA) is used to relieve various kinds of pain. However, the mechanistic basis of electroacupuncture analgesia (EAA) in inflammatory pain remains unclear. In the present study, we investigated whether endogenous peripheral corticotropin-releasing factor (CRF) or interleukin-1beta (IL-1) participated in EAA during hyperalgesia elicited by carrageenan-induced inflammation. Carrageenan was subcutaneously administered by intraplantar (i.pl.) injection of the left hind paw to induce inflammation. Nociceptive thresholds were measured using the paw pressure threshold (PPT) (Randall Sellito Test). Rats received 3 Hz EA in the left anterior tibial muscles for 1 hour after carrageenan injection. The selective CRF antagonist, alpha-helical CRF, or the recombinant IL-1 receptor antagonist, IL-1ra, was administered by i.pl. injection of the inflamed paw or by intravenous (i.v.) injection 1 hour before EA. PPT decreased significantly 3 hours after carrageenan injection. This decrease persisted at least 24 hours after carrageenan injection. EA resulted in significant increases of PPT, moreover, PPT elevations lasted 24 hours after carrageenan injection. By contrast, PPT elevations produced by EA were dose-dependently antagonized by local i.pl. injection of alpha-helical CRF or IL-1ra. This PPT elevation was not influenced by i.v. injection of alpha-helical CRF or IL-1ra. These findings suggest that peripheral CRF or IL-1 participate in EAA during hyperalgesia. The release of CRF or IL-1 elicited by EA may trigger the release of opioid peptides within inflamed tissue which may activate peripheral opioid receptors and inhibit the pain.
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