Effect of Inhibition of Prostaglandin Synthesis on Epinephrine-Induced Gastroduodenal Electromechanical Changes in Humans
We conducted a double-blind randomized study to investigate the role of endogenous prostaglandins in epinephrine-induced changes in human gastric electromechanical activity. Intravenous administration of a pharmacologic dosage of epinephrine (222 ng/kg per min) caused gastric dysrhythmia in 8 of 12...
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Veröffentlicht in: | Mayo Clinic proceedings 1989-02, Vol.64 (2), p.149-157 |
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description | We conducted a double-blind randomized study to investigate the role of endogenous prostaglandins in epinephrine-induced changes in human gastric electromechanical activity. Intravenous administration of a pharmacologic dosage of epinephrine (222 ng/kg per min) caused gastric dysrhythmia in 8 of 12 healthy subjects. After indomethacin treatment, the incidence of epinephrine-induced gastric dysrhythmia was reduced to 4 of 12 healthy subjects, which is similar to the incidence of gastric dysrhythmia noted in the placebo group. The difference, however, was not statistically significant (P = 0.2). Epinephrine also substantially inhibited both the amplitude and the frequency of antral contractions. Indomethacin treatment partially reversed the reduction in the amplitude but not the frequency of antral contractions. These results suggest that endogenous prostaglandins may, in part, regulate the amplitude of human antral contractions; however, the role of prostaglandins in epinephrine-induced gastric dysrhythmia in humans remains uncertain. |
doi_str_mv | 10.1016/S0025-6196(12)65668-7 |
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Intravenous administration of a pharmacologic dosage of epinephrine (222 ng/kg per min) caused gastric dysrhythmia in 8 of 12 healthy subjects. After indomethacin treatment, the incidence of epinephrine-induced gastric dysrhythmia was reduced to 4 of 12 healthy subjects, which is similar to the incidence of gastric dysrhythmia noted in the placebo group. The difference, however, was not statistically significant (P = 0.2). Epinephrine also substantially inhibited both the amplitude and the frequency of antral contractions. Indomethacin treatment partially reversed the reduction in the amplitude but not the frequency of antral contractions. These results suggest that endogenous prostaglandins may, in part, regulate the amplitude of human antral contractions; however, the role of prostaglandins in epinephrine-induced gastric dysrhythmia in humans remains uncertain.</description><identifier>ISSN: 0025-6196</identifier><identifier>EISSN: 1942-5546</identifier><identifier>DOI: 10.1016/S0025-6196(12)65668-7</identifier><identifier>PMID: 2921874</identifier><identifier>CODEN: MACPAJ</identifier><language>eng</language><publisher>Rochester, MN: Elsevier Inc</publisher><subject>Adult ; Biological and medical sciences ; Dose-Response Relationship, Drug ; Double-Blind Method ; Electrophysiology ; Epinephrine - pharmacology ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gastrointestinal Motility - drug effects ; Hemodynamics - drug effects ; Humans ; Indomethacin - pharmacology ; Male ; Manometry ; Mathematical Computing ; Medical sciences ; Nausea - etiology ; Other diseases. Semiology ; Prostaglandins - physiology ; Random Allocation ; Stomach - drug effects ; Stomach - physiology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><ispartof>Mayo Clinic proceedings, 1989-02, Vol.64 (2), p.149-157</ispartof><rights>1989 Mayo Foundation for Medical Education and Research</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-ccba448a2828ca98a6c4c914791824432ae96b0113bca88ef1346abf1092de373</citedby><cites>FETCH-LOGICAL-c456t-ccba448a2828ca98a6c4c914791824432ae96b0113bca88ef1346abf1092de373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19275182$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2921874$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KIM, CHUNG H.</creatorcontrib><creatorcontrib>HANSON, RUSSELL B.</creatorcontrib><creatorcontrib>ABELL, THOMAS L.</creatorcontrib><creatorcontrib>MALAGELADA, JUAN-R.</creatorcontrib><title>Effect of Inhibition of Prostaglandin Synthesis on Epinephrine-Induced Gastroduodenal Electromechanical Changes in Humans</title><title>Mayo Clinic proceedings</title><addtitle>Mayo Clin Proc</addtitle><description>We conducted a double-blind randomized study to investigate the role of endogenous prostaglandins in epinephrine-induced changes in human gastric electromechanical activity. Intravenous administration of a pharmacologic dosage of epinephrine (222 ng/kg per min) caused gastric dysrhythmia in 8 of 12 healthy subjects. After indomethacin treatment, the incidence of epinephrine-induced gastric dysrhythmia was reduced to 4 of 12 healthy subjects, which is similar to the incidence of gastric dysrhythmia noted in the placebo group. The difference, however, was not statistically significant (P = 0.2). Epinephrine also substantially inhibited both the amplitude and the frequency of antral contractions. Indomethacin treatment partially reversed the reduction in the amplitude but not the frequency of antral contractions. These results suggest that endogenous prostaglandins may, in part, regulate the amplitude of human antral contractions; however, the role of prostaglandins in epinephrine-induced gastric dysrhythmia in humans remains uncertain.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Dose-Response Relationship, Drug</subject><subject>Double-Blind Method</subject><subject>Electrophysiology</subject><subject>Epinephrine - pharmacology</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gastrointestinal Motility - drug effects</subject><subject>Hemodynamics - drug effects</subject><subject>Humans</subject><subject>Indomethacin - pharmacology</subject><subject>Male</subject><subject>Manometry</subject><subject>Mathematical Computing</subject><subject>Medical sciences</subject><subject>Nausea - etiology</subject><subject>Other diseases. Semiology</subject><subject>Prostaglandins - physiology</subject><subject>Random Allocation</subject><subject>Stomach - drug effects</subject><subject>Stomach - physiology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><issn>0025-6196</issn><issn>1942-5546</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE9r3DAQxUVJSTZpP0LAl4Tm4FSSZVk6lbJskoVAC2nPYiyPsyq2tJXswn77arNLcsxF_-bNG70fIZeM3jLK5NcnSnldSqblF8ZvZC2lKpsPZMG04GVdC3lCFq-SM3Ke0h9KaaO1OCWnXHOmGrEgu1Xfo52K0Bdrv3Gtm1zw-9vPGNIEzwP4zvniaeenDSaXilxdbZ3H7SbmtVz7brbYFfeQphi6OXToYShWQzaNYUS7Ae9sflnmwzOmIps9zCP49Il87GFI-Pm4X5Dfd6tfy4fy8cf9evn9sbSillNpbQtCKOCKKwtagbTCaiYazRQXouKAWraUsaq1oBT2rBIS2p5RzTusmuqCXB98tzH8nTFNZnTJ4pCTYZiTaZRSlZR1FtYHoc3RU8TebKMbIe4Mo2aP3LwgN3uehnHzgtzsB1weB8ztiN1r15Fxrl8d65AyiT6Cty69mWve1DlL1n076DDT-OcwmmQd-kzXxUzTdMG985P_euifXA</recordid><startdate>19890201</startdate><enddate>19890201</enddate><creator>KIM, CHUNG H.</creator><creator>HANSON, RUSSELL B.</creator><creator>ABELL, THOMAS L.</creator><creator>MALAGELADA, JUAN-R.</creator><general>Elsevier Inc</general><general>Mayo Medical Ventures</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19890201</creationdate><title>Effect of Inhibition of Prostaglandin Synthesis on Epinephrine-Induced Gastroduodenal Electromechanical Changes in Humans</title><author>KIM, CHUNG H. ; HANSON, RUSSELL B. ; ABELL, THOMAS L. ; MALAGELADA, JUAN-R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-ccba448a2828ca98a6c4c914791824432ae96b0113bca88ef1346abf1092de373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Dose-Response Relationship, Drug</topic><topic>Double-Blind Method</topic><topic>Electrophysiology</topic><topic>Epinephrine - pharmacology</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gastrointestinal Motility - drug effects</topic><topic>Hemodynamics - drug effects</topic><topic>Humans</topic><topic>Indomethacin - pharmacology</topic><topic>Male</topic><topic>Manometry</topic><topic>Mathematical Computing</topic><topic>Medical sciences</topic><topic>Nausea - etiology</topic><topic>Other diseases. Semiology</topic><topic>Prostaglandins - physiology</topic><topic>Random Allocation</topic><topic>Stomach - drug effects</topic><topic>Stomach - physiology</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KIM, CHUNG H.</creatorcontrib><creatorcontrib>HANSON, RUSSELL B.</creatorcontrib><creatorcontrib>ABELL, THOMAS L.</creatorcontrib><creatorcontrib>MALAGELADA, JUAN-R.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Mayo Clinic proceedings</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KIM, CHUNG H.</au><au>HANSON, RUSSELL B.</au><au>ABELL, THOMAS L.</au><au>MALAGELADA, JUAN-R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Inhibition of Prostaglandin Synthesis on Epinephrine-Induced Gastroduodenal Electromechanical Changes in Humans</atitle><jtitle>Mayo Clinic proceedings</jtitle><addtitle>Mayo Clin Proc</addtitle><date>1989-02-01</date><risdate>1989</risdate><volume>64</volume><issue>2</issue><spage>149</spage><epage>157</epage><pages>149-157</pages><issn>0025-6196</issn><eissn>1942-5546</eissn><coden>MACPAJ</coden><abstract>We conducted a double-blind randomized study to investigate the role of endogenous prostaglandins in epinephrine-induced changes in human gastric electromechanical activity. Intravenous administration of a pharmacologic dosage of epinephrine (222 ng/kg per min) caused gastric dysrhythmia in 8 of 12 healthy subjects. After indomethacin treatment, the incidence of epinephrine-induced gastric dysrhythmia was reduced to 4 of 12 healthy subjects, which is similar to the incidence of gastric dysrhythmia noted in the placebo group. The difference, however, was not statistically significant (P = 0.2). Epinephrine also substantially inhibited both the amplitude and the frequency of antral contractions. Indomethacin treatment partially reversed the reduction in the amplitude but not the frequency of antral contractions. These results suggest that endogenous prostaglandins may, in part, regulate the amplitude of human antral contractions; however, the role of prostaglandins in epinephrine-induced gastric dysrhythmia in humans remains uncertain.</abstract><cop>Rochester, MN</cop><pub>Elsevier Inc</pub><pmid>2921874</pmid><doi>10.1016/S0025-6196(12)65668-7</doi><tpages>9</tpages></addata></record> |
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subjects | Adult Biological and medical sciences Dose-Response Relationship, Drug Double-Blind Method Electrophysiology Epinephrine - pharmacology Female Gastroenterology. Liver. Pancreas. Abdomen Gastrointestinal Motility - drug effects Hemodynamics - drug effects Humans Indomethacin - pharmacology Male Manometry Mathematical Computing Medical sciences Nausea - etiology Other diseases. Semiology Prostaglandins - physiology Random Allocation Stomach - drug effects Stomach - physiology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus |
title | Effect of Inhibition of Prostaglandin Synthesis on Epinephrine-Induced Gastroduodenal Electromechanical Changes in Humans |
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