Jin H O, Zhou L, Lee K Y, Chang T M, Chey W Y
Department of Medicine, University of Rochester School of Medicine and Dentistry, New York 14642, USA.
Am J Physiol. 1996 Sep;271(3 Pt 1):G524-30. doi: 10.1152/ajpgi.1996.271.3.G524.
Electroacupuncture (EAP) was shown to inhibit basal gastric acid secretion in dogs and sham feeding-stimulated acid secretion in humans. However, its effect on a meal-stimulated acid secretion in dogs and the mechanisms involved remain unclear. In five dogs prepared with gastric cannulas, gastric acid secretion was determined by a dye-dilution technique for 60 min after intragastric administration of 200 ml of 4% mixed amino acid meal in six different experiments: study 1, no acupuncture; study 2, sham acupuncture (SAP); study 3, EAP; study 4, EAP plus naloxone; 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 micrograms.kg-1.h-1, respectively. EAP was performed on three different points including Pishu, ZusanLi, and Neiguan. Biphasic electrical pulse (25-100 Hz, 12-16 mA) was applied continuously via needles for 75 min starting 15 min before meal. SAP on nonacupoints in hind- and forelegs was performed with the same electrical pulse. Plasma SS, VIP, beta-endorphin, and gastrin were determined by specific radioimmunoassays. 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 changes in plasma concentration of peptides. SAP also significantly suppressed acid output (30%; P < 0.05), with a modest but significant increase in plasma beta-endorphin. However, the inhibition by EAP on the acid output was significantly greater than that by SAP (P < 0.01). Furthermore, exogenous SS (0.5 microgram.kg-1.h-1) significantly inhibited acid output (78%), whereas VIP failed to inhibit gastric acid secretion. We conclude that, in dogs, EAP significantly inhibits meal-stimulated 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-endorphin.
电针（EAP）已被证明可抑制犬的基础胃酸分泌以及人类假饲刺激引起的胃酸分泌。然而，其对犬进食刺激引起的胃酸分泌的影响及相关机制仍不清楚。在五只制备了胃插管的犬中，通过染料稀释技术在胃内给予200 ml 4%混合氨基酸餐60分钟后测定胃酸分泌，共进行了六个不同实验：实验1，无针刺；实验2，假针刺（SAP）；实验3，EAP；实验4，EAP加纳洛酮；实验5，单独使用纳洛酮；实验6，分别以0.5和1.0微克·千克⁻¹·小时⁻¹的剂量静脉输注生长抑素（SS）和血管活性肠肽（VIP）。EAP在包括脾俞、足三里和内关三个不同穴位上进行。在进食前15分钟开始，通过针持续施加双相电脉冲（25 - 100 Hz，12 - 16 mA）75分钟。在前后腿的非穴位上进行假针刺，采用相同的电脉冲。通过特异性放射免疫测定法测定血浆中的SS、VIP、β-内啡肽和胃泌素。EAP显著抑制胃酸分泌（75%；P < 0.01），这与血浆中SS、VIP和β-内啡肽的显著增加以及血浆胃泌素的显著降低相一致。纳洛酮完全逆转了EAP诱导的胃酸分泌抑制以及肽类血浆浓度的变化。假针刺也显著抑制胃酸分泌（30%；P < 0.05），血浆β-内啡肽有适度但显著的增加。然而，EAP对胃酸分泌的抑制作用明显大于假针刺（P < 0.01）。此外，外源性SS（0.5微克·千克⁻¹·小时⁻¹）显著抑制胃酸分泌（78%），而VIP未能抑制胃酸分泌。我们得出结论，在犬中，EAP显著抑制进食刺激引起的胃酸分泌。这种胃酸抑制是由β-内啡肽和生长抑素的释放介导的，并且一种或多种内源性阿片类物质似乎在SS、VIP和β-内啡肽的释放中起重要作用。
