INHIBITION OF ACID-SECRETION BY ELECTRICAL ACUPUNCTURE IS MEDIATED VIA BETA-ENDORPHIN AND SOMATOSTATIN

Electroacupuncture (EAP) was shown to inhibit basal gastric acid secre tion in dogs and sham feeding-stimulated acid secretion in humans. How ever, its effect on a meal-stimulated acid secretion in dogs and the m echanisms involved remain unclear. In five dogs prepared with gastric cannulas, gastric acid secretion was determined by a dye-dilution tech nique for 60 min after intragastric administration of 200 ml of 4% mix ed amino acid meal in six different experiments: study 1, no acupunctu re; study 2, sham acupuncture (SAP); study 3, EAP; study 4, EAP plus n aloxone; study 5, naloxone alone; and study 6, intravenous infusion of somatostatin (SS and vasoactive intestinal peptide (VIP) at doses of 0.5 and 1.0 mu g . kg(-1). h(-1), respectively. EAP was performed on t hree different points including Pishu, ZusanLi, and Neiguan. Biphasic electrical pulse (25-100 Hz, 12-16 mA) was applied continuously via ne edles for 75 min starting 15 min before meal. SAP on nonacupoints in h ind- and forelegs was performed with the same electrical pulse. Plasma SS, VIP, beta-endorphin, and gastrin were determined by specific radi oimmunoassays. EAP significantly inhibited acid secretion (75%; P < 0. 01), which coincided with significant increases in plasma SS, VIP, and beta-endorphin and a significant decrease in plasma gastrin. Naloxone completely reversed EAP-induced inhibition of acid secretion and chan ges in plasma concentration of peptides. SAP also significantly suppre ssed acid output (30%; P < 0.05), with a modest but significant increa se in plasma beta-endorphin. However, the inhibition by EAP on the aci d output was significantly greater than that by SAP (P < 0.01). Furthe rmore, exogenous SS (0.5 mu g . kg(-1). h(-1)) significantly inhibited acid output (78%), whereas VIP failed to inhibit gastric acid secreti on. We conclude that, in dogs, EAP significantly inhibits meal-stimula ted acid secretion. This acid inhibition is mediated by the release of beta-endorphin and somatostatin, and an endogenous opiate or opiates appear to play an important role in the release of SS, VIP, and beta-e ndorphin.