MECHANISM OF NEUROTOXICITY OF CARDIOTONIC GLYCOSIDES
1In cats intracerebroventricular administration of 5, 10, 20 μg of peruvoside, a cardiac glycoside obtained from the plant, Thevetia neriifolia, and 10 and 20 μg of ouabain, produced marked neurotoxicity. This was dose‐related. 2Prior administration of reserpine (2 mg/kg i.m., 500 μg i.c.v.) or tetr...
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| Veröffentlicht in: | British journal of pharmacology 1977-02, Vol.59 (2), p.223-229 |
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| creator | GAITONDÉ, B.B. JOGLEKAR, S.N. |
| description | 1In cats intracerebroventricular administration of 5, 10, 20 μg of peruvoside, a cardiac glycoside obtained from the plant, Thevetia neriifolia, and 10 and 20 μg of ouabain, produced marked neurotoxicity. This was dose‐related.
2Prior administration of reserpine (2 mg/kg i.m., 500 μg i.c.v.) or tetrabenazine (25 mg/kg i.v., 50 mg/kg i.v. and 2 mg/kg i.c.v.) suppressed the neurotoxicity, but lithium carbonate (100 mg/kg i.p., 2 mg i.c.v.) and haloperidol (200 μg i.c.v.) were ineffective.
3Prior administration of 2‐bromolysergic acid diethylamide (BOL‐148, 200 μg i.c.v.) or p‐chlorophenylalanine (PCPA) (400 mg/kg i.p.) suppressed the neurotoxicity induced by peruvoside and ouabain.
4Perfusion of the lateral ventricles of cats with 10, 20 and 30 μg of peruvoside or ouabain produced a massive release of 5‐hydroxytryptamine (5‐HT). This was dose‐related. Prior administration PCPA suppressed the release of 5‐HT.
5The results of the findings indicate the involvement of 5‐HT in the genesis of neurotoxicity induced by peruvoside or ouabain. |
| doi_str_mv | 10.1111/j.1476-5381.1977.tb07482.x |
| format | Article |
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2Prior administration of reserpine (2 mg/kg i.m., 500 μg i.c.v.) or tetrabenazine (25 mg/kg i.v., 50 mg/kg i.v. and 2 mg/kg i.c.v.) suppressed the neurotoxicity, but lithium carbonate (100 mg/kg i.p., 2 mg i.c.v.) and haloperidol (200 μg i.c.v.) were ineffective.
3Prior administration of 2‐bromolysergic acid diethylamide (BOL‐148, 200 μg i.c.v.) or p‐chlorophenylalanine (PCPA) (400 mg/kg i.p.) suppressed the neurotoxicity induced by peruvoside and ouabain.
4Perfusion of the lateral ventricles of cats with 10, 20 and 30 μg of peruvoside or ouabain produced a massive release of 5‐hydroxytryptamine (5‐HT). This was dose‐related. Prior administration PCPA suppressed the release of 5‐HT.
5The results of the findings indicate the involvement of 5‐HT in the genesis of neurotoxicity induced by peruvoside or ouabain.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/j.1476-5381.1977.tb07482.x</identifier><identifier>PMID: 13903</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Behavior, Animal - drug effects ; Brain - metabolism ; Cardenolides - pharmacology ; Cardiac Glycosides - administration & dosage ; Cardiac Glycosides - adverse effects ; Catecholamines - metabolism ; Cats ; Central Nervous System - drug effects ; Drug Interactions ; Female ; Fenclonine - pharmacology ; Haloperidol - pharmacology ; Injections, Intraventricular ; Lithium - pharmacology ; Lysergic Acid Diethylamide - pharmacology ; Male ; Ouabain - pharmacology ; Serotonin - metabolism</subject><ispartof>British journal of pharmacology, 1977-02, Vol.59 (2), p.223-229</ispartof><rights>1977 British Pharmacological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4752-1790efb8a14b6317b4767c648e970df120424138f56f0f911ab8fd050de7c69d3</citedby><cites>FETCH-LOGICAL-c4752-1790efb8a14b6317b4767c648e970df120424138f56f0f911ab8fd050de7c69d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1667725/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1667725/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/13903$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GAITONDÉ, B.B.</creatorcontrib><creatorcontrib>JOGLEKAR, S.N.</creatorcontrib><title>MECHANISM OF NEUROTOXICITY OF CARDIOTONIC GLYCOSIDES</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1In cats intracerebroventricular administration of 5, 10, 20 μg of peruvoside, a cardiac glycoside obtained from the plant, Thevetia neriifolia, and 10 and 20 μg of ouabain, produced marked neurotoxicity. This was dose‐related.
2Prior administration of reserpine (2 mg/kg i.m., 500 μg i.c.v.) or tetrabenazine (25 mg/kg i.v., 50 mg/kg i.v. and 2 mg/kg i.c.v.) suppressed the neurotoxicity, but lithium carbonate (100 mg/kg i.p., 2 mg i.c.v.) and haloperidol (200 μg i.c.v.) were ineffective.
3Prior administration of 2‐bromolysergic acid diethylamide (BOL‐148, 200 μg i.c.v.) or p‐chlorophenylalanine (PCPA) (400 mg/kg i.p.) suppressed the neurotoxicity induced by peruvoside and ouabain.
4Perfusion of the lateral ventricles of cats with 10, 20 and 30 μg of peruvoside or ouabain produced a massive release of 5‐hydroxytryptamine (5‐HT). This was dose‐related. Prior administration PCPA suppressed the release of 5‐HT.
5The results of the findings indicate the involvement of 5‐HT in the genesis of neurotoxicity induced by peruvoside or ouabain.</description><subject>Animals</subject><subject>Behavior, Animal - drug effects</subject><subject>Brain - metabolism</subject><subject>Cardenolides - pharmacology</subject><subject>Cardiac Glycosides - administration & dosage</subject><subject>Cardiac Glycosides - adverse effects</subject><subject>Catecholamines - metabolism</subject><subject>Cats</subject><subject>Central Nervous System - drug effects</subject><subject>Drug Interactions</subject><subject>Female</subject><subject>Fenclonine - pharmacology</subject><subject>Haloperidol - pharmacology</subject><subject>Injections, Intraventricular</subject><subject>Lithium - pharmacology</subject><subject>Lysergic Acid Diethylamide - pharmacology</subject><subject>Male</subject><subject>Ouabain - pharmacology</subject><subject>Serotonin - metabolism</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1977</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkFtPwjAYhhsjUUR_gTfE-83v27q180KDY8ASYIZDIlfNDq2OcMqGCv_eLhDUS3vT5nv6vm0eQu4QTNTrfm4iZa7h2BxN9Bgztwkwyi1zd0bqJ3RO6gDADETOL8lVWc4BNGTOBamh7YFdJ3QQ-L3WMBwPmlGnOQymo2gSvYZ-OJlVA781aod6Mgz9Zrc_86Nx2A7G16Sm4kUpb457g0w7wcTvGf2oG_qtvpFS5lgGMg-kSniMNHFtZIn-F0tdyqXHIFNoAbUo2lw5rgLlIcYJVxk4kEl9zcvsBnk89G4-kqXMUrnaFvFCbIp8GRd7sY5z8Zes8nfxtv4U6LqMWY4ueDgUpMW6LAupTlkEUYkUc1HZEpUtUYkUR5Fip8O3v1__iVbmNH060K98Iff_6BXPL73qZH8DNKl-rA</recordid><startdate>197702</startdate><enddate>197702</enddate><creator>GAITONDÉ, B.B.</creator><creator>JOGLEKAR, S.N.</creator><general>Blackwell Publishing Ltd</general><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>5PM</scope></search><sort><creationdate>197702</creationdate><title>MECHANISM OF NEUROTOXICITY OF CARDIOTONIC GLYCOSIDES</title><author>GAITONDÉ, B.B. ; JOGLEKAR, S.N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4752-1790efb8a14b6317b4767c648e970df120424138f56f0f911ab8fd050de7c69d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1977</creationdate><topic>Animals</topic><topic>Behavior, Animal - drug effects</topic><topic>Brain - metabolism</topic><topic>Cardenolides - pharmacology</topic><topic>Cardiac Glycosides - administration & dosage</topic><topic>Cardiac Glycosides - adverse effects</topic><topic>Catecholamines - metabolism</topic><topic>Cats</topic><topic>Central Nervous System - drug effects</topic><topic>Drug Interactions</topic><topic>Female</topic><topic>Fenclonine - pharmacology</topic><topic>Haloperidol - pharmacology</topic><topic>Injections, Intraventricular</topic><topic>Lithium - pharmacology</topic><topic>Lysergic Acid Diethylamide - pharmacology</topic><topic>Male</topic><topic>Ouabain - pharmacology</topic><topic>Serotonin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GAITONDÉ, B.B.</creatorcontrib><creatorcontrib>JOGLEKAR, S.N.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GAITONDÉ, B.B.</au><au>JOGLEKAR, S.N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MECHANISM OF NEUROTOXICITY OF CARDIOTONIC GLYCOSIDES</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1977-02</date><risdate>1977</risdate><volume>59</volume><issue>2</issue><spage>223</spage><epage>229</epage><pages>223-229</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><abstract>1In cats intracerebroventricular administration of 5, 10, 20 μg of peruvoside, a cardiac glycoside obtained from the plant, Thevetia neriifolia, and 10 and 20 μg of ouabain, produced marked neurotoxicity. This was dose‐related.
2Prior administration of reserpine (2 mg/kg i.m., 500 μg i.c.v.) or tetrabenazine (25 mg/kg i.v., 50 mg/kg i.v. and 2 mg/kg i.c.v.) suppressed the neurotoxicity, but lithium carbonate (100 mg/kg i.p., 2 mg i.c.v.) and haloperidol (200 μg i.c.v.) were ineffective.
3Prior administration of 2‐bromolysergic acid diethylamide (BOL‐148, 200 μg i.c.v.) or p‐chlorophenylalanine (PCPA) (400 mg/kg i.p.) suppressed the neurotoxicity induced by peruvoside and ouabain.
4Perfusion of the lateral ventricles of cats with 10, 20 and 30 μg of peruvoside or ouabain produced a massive release of 5‐hydroxytryptamine (5‐HT). This was dose‐related. Prior administration PCPA suppressed the release of 5‐HT.
5The results of the findings indicate the involvement of 5‐HT in the genesis of neurotoxicity induced by peruvoside or ouabain.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>13903</pmid><doi>10.1111/j.1476-5381.1977.tb07482.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Behavior, Animal - drug effects Brain - metabolism Cardenolides - pharmacology Cardiac Glycosides - administration & dosage Cardiac Glycosides - adverse effects Catecholamines - metabolism Cats Central Nervous System - drug effects Drug Interactions Female Fenclonine - pharmacology Haloperidol - pharmacology Injections, Intraventricular Lithium - pharmacology Lysergic Acid Diethylamide - pharmacology Male Ouabain - pharmacology Serotonin - metabolism |
| title | MECHANISM OF NEUROTOXICITY OF CARDIOTONIC GLYCOSIDES |
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