| Inhibition of acid secretion by electrical acupuncture is mediated via beta-endorphin and somatostatin. | |
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MedLine Citation:
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PMID: 8843779 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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H O Jin; L Zhou; K Y Lee; T M Chang; W Y Chey |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The American journal of physiology Volume: 271 ISSN: 0002-9513 ISO Abbreviation: Am. J. Physiol. Publication Date: 1996 Sep |
Date Detail:
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Created Date: 1996-12-05 Completed Date: 1996-12-05 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0370511 Medline TA: Am J Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: G524-30 Citation Subset: IM |
Affiliation:
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Department of Medicine, University of Rochester School of Medicine and Dentistry, New York 14642, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acupuncture Therapy Animals Dogs Gastric Acid / secretion* Somatostatin / metabolism* Stomach / innervation, metabolism* beta-Endorphin / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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DK-25692/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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51110-01-1/Somatostatin; 60617-12-1/beta-Endorphin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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