Involvement of nitric oxide and prostaglandins in gastric mucosal hyperemia of portal‐hypertensive anesthetized rats
This study investigates the effects of inhibition of nitric oxide synthesis by NG‐nitro‐L‐arginine methyl ester (L‐NAME), the inhibition of prostaglandin synthesis with indomethacin and the combined effects on gastric mucosal hyperemia of ketamine‐anesthetized rats with portal hypertension induced b...
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Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 1993-09, Vol.18 (3), p.628-634 |
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creator | Casadevall, María Panés, Julián Piqué, Josep M. Marroni, Norma Bosch, Jaume Whittle, Brendan J. R. |
description | This study investigates the effects of inhibition of nitric oxide synthesis by NG‐nitro‐L‐arginine methyl ester (L‐NAME), the inhibition of prostaglandin synthesis with indomethacin and the combined effects on gastric mucosal hyperemia of ketamine‐anesthetized rats with portal hypertension induced by partial portal vein ligation. The hydrogen gas–clearance technique was used for measurement of gastric mucosal blood flow. Blood pressure increased with L‐NAME administration in a similar manner in portal‐hypertensive and sham‐operated rats. Low doses of L‐NAME (1 and 3 mg/kg, intravenously) caused a significant and dosedependent reduction in gastric mucosal blood flow in portal‐hypertensive rats but had no effect on shamoperated animals. With a higher dose of L‐NAME (13 mg/kg, intravenously), a significant decrease in gastric mucosal blood flow was observed in both portal‐hypertensive and sham‐operated rats. Indomethacin pretreatment (5 mg/kg, subcutaneously) caused a significant decrease in basal gastric mucosal blood flow of portal‐hypertensive rats but did not modify this parameter in sham‐operated animals. In sham‐operated rats pretreated with indomethacin, the lower dose of L‐NAME (3 mg/kg) did not significantly modify basal gastric mucosal blood flow. Likewise, pretreatment with indomethacin in sham‐operated rats did not augment the significant reduction in gastric mucosal blood flow produced by the higher dose of L‐NAME. In portal‐hypertensive rats the significant dose‐dependent reduction in gastric mucosal blood flow induced by L‐NAME (3 and 13 mg/kg) was not significantly altered by pretreatment with indomethacin. Portal pressure was higher in portal‐hypertensive than in sham‐operated rats, and no significant differences were observed in this parameter between portal‐hypertensive animals treated with different doses of L‐NAME. These results indicate that both nitric oxide and prostaglandins may be involved in the gastric mucosal hyperemia of portal‐hypertensive rats. However, no synergistic interactions between these two endogenous vasodilators could be observed in this experimental model. (HEPATOLOGY 1993;18:628–634.) |
doi_str_mv | 10.1002/hep.1840180323 |
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R.</creator><creatorcontrib>Casadevall, María ; Panés, Julián ; Piqué, Josep M. ; Marroni, Norma ; Bosch, Jaume ; Whittle, Brendan J. R.</creatorcontrib><description>This study investigates the effects of inhibition of nitric oxide synthesis by NG‐nitro‐L‐arginine methyl ester (L‐NAME), the inhibition of prostaglandin synthesis with indomethacin and the combined effects on gastric mucosal hyperemia of ketamine‐anesthetized rats with portal hypertension induced by partial portal vein ligation. The hydrogen gas–clearance technique was used for measurement of gastric mucosal blood flow. Blood pressure increased with L‐NAME administration in a similar manner in portal‐hypertensive and sham‐operated rats. Low doses of L‐NAME (1 and 3 mg/kg, intravenously) caused a significant and dosedependent reduction in gastric mucosal blood flow in portal‐hypertensive rats but had no effect on shamoperated animals. With a higher dose of L‐NAME (13 mg/kg, intravenously), a significant decrease in gastric mucosal blood flow was observed in both portal‐hypertensive and sham‐operated rats. Indomethacin pretreatment (5 mg/kg, subcutaneously) caused a significant decrease in basal gastric mucosal blood flow of portal‐hypertensive rats but did not modify this parameter in sham‐operated animals. In sham‐operated rats pretreated with indomethacin, the lower dose of L‐NAME (3 mg/kg) did not significantly modify basal gastric mucosal blood flow. Likewise, pretreatment with indomethacin in sham‐operated rats did not augment the significant reduction in gastric mucosal blood flow produced by the higher dose of L‐NAME. In portal‐hypertensive rats the significant dose‐dependent reduction in gastric mucosal blood flow induced by L‐NAME (3 and 13 mg/kg) was not significantly altered by pretreatment with indomethacin. Portal pressure was higher in portal‐hypertensive than in sham‐operated rats, and no significant differences were observed in this parameter between portal‐hypertensive animals treated with different doses of L‐NAME. These results indicate that both nitric oxide and prostaglandins may be involved in the gastric mucosal hyperemia of portal‐hypertensive rats. However, no synergistic interactions between these two endogenous vasodilators could be observed in this experimental model. (HEPATOLOGY 1993;18:628–634.)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.1840180323</identifier><identifier>PMID: 8359804</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Philadelphia, PA: W.B. Saunders</publisher><subject>Anesthesia, General ; Animals ; Arginine - analogs & derivatives ; Arginine - pharmacology ; Biological and medical sciences ; Blood Pressure - drug effects ; Gastric Mucosa - blood supply ; Gastroenterology. Liver. Pancreas. Abdomen ; Hypertension, Portal - metabolism ; Hypertension, Portal - physiopathology ; Indomethacin - pharmacology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; NG-Nitroarginine Methyl Ester ; Nitric Oxide - metabolism ; Other diseases. Semiology ; Prostaglandins - metabolism ; Rats ; Rats, Sprague-Dawley ; Reference Values ; Regional Blood Flow - drug effects</subject><ispartof>Hepatology (Baltimore, Md.), 1993-09, Vol.18 (3), p.628-634</ispartof><rights>Copyright © 1993 American Association for the Study of Liver Diseases</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4353-675f6bb60cc2e718427e628e747e4fded974628f564d474dd13661da50d956e23</citedby><cites>FETCH-LOGICAL-c4353-675f6bb60cc2e718427e628e747e4fded974628f564d474dd13661da50d956e23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.1840180323$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.1840180323$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3827244$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8359804$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Casadevall, María</creatorcontrib><creatorcontrib>Panés, Julián</creatorcontrib><creatorcontrib>Piqué, Josep M.</creatorcontrib><creatorcontrib>Marroni, Norma</creatorcontrib><creatorcontrib>Bosch, Jaume</creatorcontrib><creatorcontrib>Whittle, Brendan J. R.</creatorcontrib><title>Involvement of nitric oxide and prostaglandins in gastric mucosal hyperemia of portal‐hypertensive anesthetized rats</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>This study investigates the effects of inhibition of nitric oxide synthesis by NG‐nitro‐L‐arginine methyl ester (L‐NAME), the inhibition of prostaglandin synthesis with indomethacin and the combined effects on gastric mucosal hyperemia of ketamine‐anesthetized rats with portal hypertension induced by partial portal vein ligation. The hydrogen gas–clearance technique was used for measurement of gastric mucosal blood flow. Blood pressure increased with L‐NAME administration in a similar manner in portal‐hypertensive and sham‐operated rats. Low doses of L‐NAME (1 and 3 mg/kg, intravenously) caused a significant and dosedependent reduction in gastric mucosal blood flow in portal‐hypertensive rats but had no effect on shamoperated animals. With a higher dose of L‐NAME (13 mg/kg, intravenously), a significant decrease in gastric mucosal blood flow was observed in both portal‐hypertensive and sham‐operated rats. Indomethacin pretreatment (5 mg/kg, subcutaneously) caused a significant decrease in basal gastric mucosal blood flow of portal‐hypertensive rats but did not modify this parameter in sham‐operated animals. In sham‐operated rats pretreated with indomethacin, the lower dose of L‐NAME (3 mg/kg) did not significantly modify basal gastric mucosal blood flow. Likewise, pretreatment with indomethacin in sham‐operated rats did not augment the significant reduction in gastric mucosal blood flow produced by the higher dose of L‐NAME. In portal‐hypertensive rats the significant dose‐dependent reduction in gastric mucosal blood flow induced by L‐NAME (3 and 13 mg/kg) was not significantly altered by pretreatment with indomethacin. Portal pressure was higher in portal‐hypertensive than in sham‐operated rats, and no significant differences were observed in this parameter between portal‐hypertensive animals treated with different doses of L‐NAME. These results indicate that both nitric oxide and prostaglandins may be involved in the gastric mucosal hyperemia of portal‐hypertensive rats. However, no synergistic interactions between these two endogenous vasodilators could be observed in this experimental model. (HEPATOLOGY 1993;18:628–634.)</description><subject>Anesthesia, General</subject><subject>Animals</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Gastric Mucosa - blood supply</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hypertension, Portal - metabolism</subject><subject>Hypertension, Portal - physiopathology</subject><subject>Indomethacin - pharmacology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>NG-Nitroarginine Methyl Ester</subject><subject>Nitric Oxide - metabolism</subject><subject>Other diseases. Semiology</subject><subject>Prostaglandins - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reference Values</subject><subject>Regional Blood Flow - drug effects</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtOGzEUhq2KCgJ02x2SF4jdBN89s0RRaCIhlUVZjxz7DHE1t9qT0HTVR-gz9knwkCjtjpUv5zv_Of-P0GdKppQQdruGfkpzQWhOOOMf0IRKpjPOJTlBE8I0yQrKizN0HuN3QkghWH6KTnMui5yICdou221Xb6GBdsBdhVs_BG9x99M7wKZ1uA9dHMxzne6-jdi3-NnEN6bZ2C6aGq93PQRovBn7-y4Mpv77-8_b7wBt9NtRCOKwhsH_AoeDGeIl-liZOsKnw3mBnu7n32aL7OHrl-Xs7iGzgkueKS0rtVopYi0DnWwyDYrloIUGUTlwhRbpXUklnNDCOcqVos5I4gqpgPELdLPXTTZ-bNISZeOjhTrZgW4TSy0LphVXCZzuQZv8xgBV2QffmLArKSnHoMsUdPkv6NRwdVDerBpwR_yQbKpfH-omWlNXwbTWxyPGc6aZGLFij734GnbvDC0X88f_VngFoIWZ3g</recordid><startdate>199309</startdate><enddate>199309</enddate><creator>Casadevall, María</creator><creator>Panés, Julián</creator><creator>Piqué, Josep M.</creator><creator>Marroni, Norma</creator><creator>Bosch, Jaume</creator><creator>Whittle, Brendan J. R.</creator><general>W.B. Saunders</general><general>Wiley</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>199309</creationdate><title>Involvement of nitric oxide and prostaglandins in gastric mucosal hyperemia of portal‐hypertensive anesthetized rats</title><author>Casadevall, María ; Panés, Julián ; Piqué, Josep M. ; Marroni, Norma ; Bosch, Jaume ; Whittle, Brendan J. R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4353-675f6bb60cc2e718427e628e747e4fded974628f564d474dd13661da50d956e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Anesthesia, General</topic><topic>Animals</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Gastric Mucosa - blood supply</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hypertension, Portal - metabolism</topic><topic>Hypertension, Portal - physiopathology</topic><topic>Indomethacin - pharmacology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>NG-Nitroarginine Methyl Ester</topic><topic>Nitric Oxide - metabolism</topic><topic>Other diseases. Semiology</topic><topic>Prostaglandins - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reference Values</topic><topic>Regional Blood Flow - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Casadevall, María</creatorcontrib><creatorcontrib>Panés, Julián</creatorcontrib><creatorcontrib>Piqué, Josep M.</creatorcontrib><creatorcontrib>Marroni, Norma</creatorcontrib><creatorcontrib>Bosch, Jaume</creatorcontrib><creatorcontrib>Whittle, Brendan J. 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>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Casadevall, María</au><au>Panés, Julián</au><au>Piqué, Josep M.</au><au>Marroni, Norma</au><au>Bosch, Jaume</au><au>Whittle, Brendan J. R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of nitric oxide and prostaglandins in gastric mucosal hyperemia of portal‐hypertensive anesthetized rats</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>1993-09</date><risdate>1993</risdate><volume>18</volume><issue>3</issue><spage>628</spage><epage>634</epage><pages>628-634</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>This study investigates the effects of inhibition of nitric oxide synthesis by NG‐nitro‐L‐arginine methyl ester (L‐NAME), the inhibition of prostaglandin synthesis with indomethacin and the combined effects on gastric mucosal hyperemia of ketamine‐anesthetized rats with portal hypertension induced by partial portal vein ligation. The hydrogen gas–clearance technique was used for measurement of gastric mucosal blood flow. Blood pressure increased with L‐NAME administration in a similar manner in portal‐hypertensive and sham‐operated rats. Low doses of L‐NAME (1 and 3 mg/kg, intravenously) caused a significant and dosedependent reduction in gastric mucosal blood flow in portal‐hypertensive rats but had no effect on shamoperated animals. With a higher dose of L‐NAME (13 mg/kg, intravenously), a significant decrease in gastric mucosal blood flow was observed in both portal‐hypertensive and sham‐operated rats. Indomethacin pretreatment (5 mg/kg, subcutaneously) caused a significant decrease in basal gastric mucosal blood flow of portal‐hypertensive rats but did not modify this parameter in sham‐operated animals. In sham‐operated rats pretreated with indomethacin, the lower dose of L‐NAME (3 mg/kg) did not significantly modify basal gastric mucosal blood flow. Likewise, pretreatment with indomethacin in sham‐operated rats did not augment the significant reduction in gastric mucosal blood flow produced by the higher dose of L‐NAME. In portal‐hypertensive rats the significant dose‐dependent reduction in gastric mucosal blood flow induced by L‐NAME (3 and 13 mg/kg) was not significantly altered by pretreatment with indomethacin. Portal pressure was higher in portal‐hypertensive than in sham‐operated rats, and no significant differences were observed in this parameter between portal‐hypertensive animals treated with different doses of L‐NAME. These results indicate that both nitric oxide and prostaglandins may be involved in the gastric mucosal hyperemia of portal‐hypertensive rats. However, no synergistic interactions between these two endogenous vasodilators could be observed in this experimental model. (HEPATOLOGY 1993;18:628–634.)</abstract><cop>Philadelphia, PA</cop><pub>W.B. Saunders</pub><pmid>8359804</pmid><doi>10.1002/hep.1840180323</doi><tpages>7</tpages></addata></record> |
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subjects | Anesthesia, General Animals Arginine - analogs & derivatives Arginine - pharmacology Biological and medical sciences Blood Pressure - drug effects Gastric Mucosa - blood supply Gastroenterology. Liver. Pancreas. Abdomen Hypertension, Portal - metabolism Hypertension, Portal - physiopathology Indomethacin - pharmacology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences NG-Nitroarginine Methyl Ester Nitric Oxide - metabolism Other diseases. Semiology Prostaglandins - metabolism Rats Rats, Sprague-Dawley Reference Values Regional Blood Flow - drug effects |
title | Involvement of nitric oxide and prostaglandins in gastric mucosal hyperemia of portal‐hypertensive anesthetized rats |
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