Apomorphine-induced myocardial protection is due to antioxidant and not adrenergic/dopaminergic effects
Apomorphine (Apo), a dopaminergic agonist used for treatment of Parkinson disease, is a potent antioxidant. In addition to its antioxidative effects, the dopaminergic and adrenergic effects of Apo were studied. Isolated perfused rat hearts were exposed to 25 min of no-flow global ischemia (37°C) and...
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| creator | Khaliulin, Igor Schneider, Aviva Houminer, Esther Borman, Joseph B. Schwalb, Herzl |
| description | Apomorphine (Apo), a dopaminergic agonist used for treatment of Parkinson disease, is a potent antioxidant. In addition to its antioxidative effects, the dopaminergic and adrenergic effects of Apo were studied. Isolated perfused rat hearts were exposed to 25 min of no-flow global ischemia (37°C) and 60 min of reperfusion (I/R, control). Drugs were introduced for the first 20 min of reperfusion. The LVDP of the control group recovered to 54.6 ± 3.3%. Apo-treated hearts had significantly improved recovery (61.6 ± 5%,
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| doi_str_mv | 10.1016/j.freeradbiomed.2006.01.001 |
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p < 0.05). The recovery of the work index LVDP × HR was even bigger: 67.8 ± 3.7% (Apo treatment) vs 41.7 ± 4.6% (control,
p < 0.001). Haloperidol, a dopaminergic antagonist, did not affect the recovery with Apo. Propranolol, a β-adrenergic blocker, initially inhibited the effect of Apo. However, the recovery of the combined group (Apo + propranolol) increased and reached significance (LVDP,
p < 0.05 vs control group) after cessation of propranolol perfusion. At 60 min of reperfusion this group was superior to Apo-treated hearts (LVDP,
p < 0.05). Propranolol (without Apo) did not improve the hemodynamic recovery. The same pattern of recovery applies also to the recovery of the +
dP/dt during the reperfusion.
l-DOPA was less effective than Apo. I/R caused significant increase in carbonylation of proteins. Apomorphine inhibited the increase in carbonylation. Haloperidol did not affect this beneficial effect of Apo.
l-DOPA significantly decreased the carbonylation of proteins. We conclude that the antioxidative effect of Apo is its main mechanism of cardioprotection.</description><identifier>ISSN: 0891-5849</identifier><identifier>EISSN: 1873-4596</identifier><identifier>DOI: 10.1016/j.freeradbiomed.2006.01.001</identifier><identifier>PMID: 16678010</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adrenergic Agents - pharmacology ; Animals ; Antioxidants - pharmacology ; Apomorphine - pharmacology ; Carbonyls ; Dopamine Agents - pharmacology ; Electrophoresis, Polyacrylamide Gel ; Free radicals ; Haloperidol ; Haloperidol - pharmacology ; Heart ; Heart - drug effects ; Hemodynamics - drug effects ; Immunoblotting ; Ischemia ; l-DOPA ; Levodopa - pharmacology ; Male ; Myocardial Reperfusion Injury - drug therapy ; Propranolol ; Propranolol - pharmacology ; Rats ; Rats, Sprague-Dawley</subject><ispartof>Free radical biology & medicine, 2006-05, Vol.40 (10), p.1713-1720</ispartof><rights>2006 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-c9aeff9d353f2dd597f875ac0a856e2c001ea5efd6841b14a9e2f971ef484acf3</citedby><cites>FETCH-LOGICAL-c412t-c9aeff9d353f2dd597f875ac0a856e2c001ea5efd6841b14a9e2f971ef484acf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0891584906000049$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16678010$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Khaliulin, Igor</creatorcontrib><creatorcontrib>Schneider, Aviva</creatorcontrib><creatorcontrib>Houminer, Esther</creatorcontrib><creatorcontrib>Borman, Joseph B.</creatorcontrib><creatorcontrib>Schwalb, Herzl</creatorcontrib><title>Apomorphine-induced myocardial protection is due to antioxidant and not adrenergic/dopaminergic effects</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>Apomorphine (Apo), a dopaminergic agonist used for treatment of Parkinson disease, is a potent antioxidant. In addition to its antioxidative effects, the dopaminergic and adrenergic effects of Apo were studied. Isolated perfused rat hearts were exposed to 25 min of no-flow global ischemia (37°C) and 60 min of reperfusion (I/R, control). Drugs were introduced for the first 20 min of reperfusion. The LVDP of the control group recovered to 54.6 ± 3.3%. Apo-treated hearts had significantly improved recovery (61.6 ± 5%,
p < 0.05). The recovery of the work index LVDP × HR was even bigger: 67.8 ± 3.7% (Apo treatment) vs 41.7 ± 4.6% (control,
p < 0.001). Haloperidol, a dopaminergic antagonist, did not affect the recovery with Apo. Propranolol, a β-adrenergic blocker, initially inhibited the effect of Apo. However, the recovery of the combined group (Apo + propranolol) increased and reached significance (LVDP,
p < 0.05 vs control group) after cessation of propranolol perfusion. At 60 min of reperfusion this group was superior to Apo-treated hearts (LVDP,
p < 0.05). Propranolol (without Apo) did not improve the hemodynamic recovery. The same pattern of recovery applies also to the recovery of the +
dP/dt during the reperfusion.
l-DOPA was less effective than Apo. I/R caused significant increase in carbonylation of proteins. Apomorphine inhibited the increase in carbonylation. Haloperidol did not affect this beneficial effect of Apo.
l-DOPA significantly decreased the carbonylation of proteins. We conclude that the antioxidative effect of Apo is its main mechanism of cardioprotection.</description><subject>Adrenergic Agents - pharmacology</subject><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Apomorphine - pharmacology</subject><subject>Carbonyls</subject><subject>Dopamine Agents - pharmacology</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Free radicals</subject><subject>Haloperidol</subject><subject>Haloperidol - pharmacology</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Hemodynamics - drug effects</subject><subject>Immunoblotting</subject><subject>Ischemia</subject><subject>l-DOPA</subject><subject>Levodopa - pharmacology</subject><subject>Male</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Propranolol</subject><subject>Propranolol - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>0891-5849</issn><issn>1873-4596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUctKAzEUDaLYWv0FGRDczZjMI5PgqpT6gIIbXYc0uakpncmYzIj9ezO0CK6ULE6Se859HYRuCM4IJvRumxkP4KVeW9eAznKMaYZJhjE5QVPC6iItK05P0RQzTtKKlXyCLkLYYozLqmDnaEIorRkmeIo28841znfvtoXUtnpQoJNm75T02spd0nnXg-qtaxMbEj1A0rtEtvHjy-qI8a6T1kXUHlrwG6vutOtkYw-PBIyJ-nCJzozcBbg64gy9PSxfF0_p6uXxeTFfpaokeZ8qLqOA66IqTK51xWvD6koqLFlFIVdxRpAVGE1ZSdaklBxyw2sCpmSlVKaYodtD3tj4xwChF40NCnY72YIbgqA1L1hO6z-JpB4PpZF4fyAq70LwYETnbSP9XhAsRkPEVvwyRIyGCExEbDaqr49lhvUY-9EeHYiE5YEAcSufFrwIykIbbbA-Lk5oZ_9V6BvWhqcc</recordid><startdate>20060515</startdate><enddate>20060515</enddate><creator>Khaliulin, Igor</creator><creator>Schneider, Aviva</creator><creator>Houminer, Esther</creator><creator>Borman, Joseph B.</creator><creator>Schwalb, Herzl</creator><general>Elsevier Inc</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20060515</creationdate><title>Apomorphine-induced myocardial protection is due to antioxidant and not adrenergic/dopaminergic effects</title><author>Khaliulin, Igor ; Schneider, Aviva ; Houminer, Esther ; Borman, Joseph B. ; Schwalb, Herzl</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-c9aeff9d353f2dd597f875ac0a856e2c001ea5efd6841b14a9e2f971ef484acf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adrenergic Agents - pharmacology</topic><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Apomorphine - pharmacology</topic><topic>Carbonyls</topic><topic>Dopamine Agents - pharmacology</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Free radicals</topic><topic>Haloperidol</topic><topic>Haloperidol - pharmacology</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Hemodynamics - drug effects</topic><topic>Immunoblotting</topic><topic>Ischemia</topic><topic>l-DOPA</topic><topic>Levodopa - pharmacology</topic><topic>Male</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Propranolol</topic><topic>Propranolol - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Khaliulin, Igor</creatorcontrib><creatorcontrib>Schneider, Aviva</creatorcontrib><creatorcontrib>Houminer, Esther</creatorcontrib><creatorcontrib>Borman, Joseph B.</creatorcontrib><creatorcontrib>Schwalb, Herzl</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khaliulin, Igor</au><au>Schneider, Aviva</au><au>Houminer, Esther</au><au>Borman, Joseph B.</au><au>Schwalb, Herzl</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apomorphine-induced myocardial protection is due to antioxidant and not adrenergic/dopaminergic effects</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>2006-05-15</date><risdate>2006</risdate><volume>40</volume><issue>10</issue><spage>1713</spage><epage>1720</epage><pages>1713-1720</pages><issn>0891-5849</issn><eissn>1873-4596</eissn><abstract>Apomorphine (Apo), a dopaminergic agonist used for treatment of Parkinson disease, is a potent antioxidant. In addition to its antioxidative effects, the dopaminergic and adrenergic effects of Apo were studied. Isolated perfused rat hearts were exposed to 25 min of no-flow global ischemia (37°C) and 60 min of reperfusion (I/R, control). Drugs were introduced for the first 20 min of reperfusion. The LVDP of the control group recovered to 54.6 ± 3.3%. Apo-treated hearts had significantly improved recovery (61.6 ± 5%,
p < 0.05). The recovery of the work index LVDP × HR was even bigger: 67.8 ± 3.7% (Apo treatment) vs 41.7 ± 4.6% (control,
p < 0.001). Haloperidol, a dopaminergic antagonist, did not affect the recovery with Apo. Propranolol, a β-adrenergic blocker, initially inhibited the effect of Apo. However, the recovery of the combined group (Apo + propranolol) increased and reached significance (LVDP,
p < 0.05 vs control group) after cessation of propranolol perfusion. At 60 min of reperfusion this group was superior to Apo-treated hearts (LVDP,
p < 0.05). Propranolol (without Apo) did not improve the hemodynamic recovery. The same pattern of recovery applies also to the recovery of the +
dP/dt during the reperfusion.
l-DOPA was less effective than Apo. I/R caused significant increase in carbonylation of proteins. Apomorphine inhibited the increase in carbonylation. Haloperidol did not affect this beneficial effect of Apo.
l-DOPA significantly decreased the carbonylation of proteins. We conclude that the antioxidative effect of Apo is its main mechanism of cardioprotection.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16678010</pmid><doi>10.1016/j.freeradbiomed.2006.01.001</doi><tpages>8</tpages></addata></record> |
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| subjects | Adrenergic Agents - pharmacology Animals Antioxidants - pharmacology Apomorphine - pharmacology Carbonyls Dopamine Agents - pharmacology Electrophoresis, Polyacrylamide Gel Free radicals Haloperidol Haloperidol - pharmacology Heart Heart - drug effects Hemodynamics - drug effects Immunoblotting Ischemia l-DOPA Levodopa - pharmacology Male Myocardial Reperfusion Injury - drug therapy Propranolol Propranolol - pharmacology Rats Rats, Sprague-Dawley |
| title | Apomorphine-induced myocardial protection is due to antioxidant and not adrenergic/dopaminergic effects |
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