Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial KATP channel
This study was designed to investigate the anti-arrhythmic effect of diosgenin preconditioning in myocardial reperfusion injury in rat, focusing on the involvement of the nitric oxide (NO) system and mitochondrial ATP-dependent potassium (mitoKATP) channels in this scenario. After isolation of the h...
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| Veröffentlicht in: | The journal of physiological sciences 2014-11, Vol.64 (6), p.393-400 |
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| creator | Badalzadeh, Reza Yousefi, Bahman Majidinia, Maryam Ebrahimi, Hadi |
| description | This study was designed to investigate the anti-arrhythmic effect of diosgenin preconditioning in myocardial reperfusion injury in rat, focusing on the involvement of the nitric oxide (NO) system and mitochondrial ATP-dependent potassium (mitoKATP) channels in this scenario. After isolation of the hearts of male Wister rats, the study was conducted in an isolated buffer-perfused heart model. Global ischemia (for 30 min) was induced by interruption of the aortic supply, which was followed by 90-min reperfusion. Throughout the experiment, the electrocardiograms of hearts were monitored using three golden surface electrodes connected to a data acquisition system. Arrhythmias were assessed based on the Lambeth convention and were categorized as number, duration and incidence of ventricular tachycardia (VT), ventricular fibrillation (VF), and premature ventricular complexes (PVC), and arrhythmic score. Additionally, lactate dehydrogenase (LDH) levels in coronary effluent were estimated colorimetrically. Diosgenin pre-administration for 20 min before ischemia reduced the LDH release into the coronary effluent, as compared with control hearts (P |
| doi_str_mv | 10.1007/s12576-014-0333-8 |
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After isolation of the hearts of male Wister rats, the study was conducted in an isolated buffer-perfused heart model. Global ischemia (for 30 min) was induced by interruption of the aortic supply, which was followed by 90-min reperfusion. Throughout the experiment, the electrocardiograms of hearts were monitored using three golden surface electrodes connected to a data acquisition system. Arrhythmias were assessed based on the Lambeth convention and were categorized as number, duration and incidence of ventricular tachycardia (VT), ventricular fibrillation (VF), and premature ventricular complexes (PVC), and arrhythmic score. Additionally, lactate dehydrogenase (LDH) levels in coronary effluent were estimated colorimetrically. Diosgenin pre-administration for 20 min before ischemia reduced the LDH release into the coronary effluent, as compared with control hearts (P < 0.05). In addition, the diosgenin-receiving group showed a lower number of PVC, VT and VF, a reduced duration and incidence of VT and VF, and less severe arrhythmia at reperfusion phase, in comparison with controls. Blocking the mitoKATP channels using 5-hydroxydecanoate as well as inhibiting the NO system through prior administration of L-NAME significantly reduced the positive effects of diosgenin. Our finding showed that pre-administration of diosgenin could provide cardioprotection through anti-arrhythmic effects against ischemia-reperfusion (I/R) injury in isolated rat hearts. In addition, mitoKATP channels and NO system may be the key players in diosgenin-induced cardioprotective mechanisms.</description><identifier>ISSN: 1880-6546</identifier><identifier>EISSN: 1880-6562</identifier><identifier>DOI: 10.1007/s12576-014-0333-8</identifier><identifier>PMID: 25150984</identifier><language>eng</language><publisher>Japan: Springer Japan</publisher><subject>Animals ; Anti-Arrhythmia Agents - pharmacology ; Arrhythmias, Cardiac - drug therapy ; Arrhythmias, Cardiac - metabolism ; Cardiotonic Agents - pharmacology ; Decanoic Acids - pharmacology ; Diosgenin - pharmacology ; Heart - drug effects ; Hydroxy Acids - pharmacology ; L-Lactate Dehydrogenase - metabolism ; Male ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - metabolism ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide - metabolism ; Original Paper ; Potassium Channels - metabolism ; Rats ; Rats, Wistar ; Tachycardia, Ventricular - drug therapy ; Tachycardia, Ventricular - metabolism ; Ventricular Fibrillation - drug therapy ; Ventricular Fibrillation - metabolism</subject><ispartof>The journal of physiological sciences, 2014-11, Vol.64 (6), p.393-400</ispartof><rights>The Physiological Society of Japan and Springer Japan 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3728-586f9c58491165c3af44f1276c36c5dcc093e9284334e60fa1dc9de94f5d4b683</citedby><cites>FETCH-LOGICAL-c3728-586f9c58491165c3af44f1276c36c5dcc093e9284334e60fa1dc9de94f5d4b683</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/PMC10717021/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717021/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25150984$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Badalzadeh, Reza</creatorcontrib><creatorcontrib>Yousefi, Bahman</creatorcontrib><creatorcontrib>Majidinia, Maryam</creatorcontrib><creatorcontrib>Ebrahimi, Hadi</creatorcontrib><title>Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial KATP channel</title><title>The journal of physiological sciences</title><addtitle>J Physiol Sci</addtitle><description>This study was designed to investigate the anti-arrhythmic effect of diosgenin preconditioning in myocardial reperfusion injury in rat, focusing on the involvement of the nitric oxide (NO) system and mitochondrial ATP-dependent potassium (mitoKATP) channels in this scenario. After isolation of the hearts of male Wister rats, the study was conducted in an isolated buffer-perfused heart model. Global ischemia (for 30 min) was induced by interruption of the aortic supply, which was followed by 90-min reperfusion. Throughout the experiment, the electrocardiograms of hearts were monitored using three golden surface electrodes connected to a data acquisition system. Arrhythmias were assessed based on the Lambeth convention and were categorized as number, duration and incidence of ventricular tachycardia (VT), ventricular fibrillation (VF), and premature ventricular complexes (PVC), and arrhythmic score. Additionally, lactate dehydrogenase (LDH) levels in coronary effluent were estimated colorimetrically. Diosgenin pre-administration for 20 min before ischemia reduced the LDH release into the coronary effluent, as compared with control hearts (P < 0.05). In addition, the diosgenin-receiving group showed a lower number of PVC, VT and VF, a reduced duration and incidence of VT and VF, and less severe arrhythmia at reperfusion phase, in comparison with controls. Blocking the mitoKATP channels using 5-hydroxydecanoate as well as inhibiting the NO system through prior administration of L-NAME significantly reduced the positive effects of diosgenin. Our finding showed that pre-administration of diosgenin could provide cardioprotection through anti-arrhythmic effects against ischemia-reperfusion (I/R) injury in isolated rat hearts. In addition, mitoKATP channels and NO system may be the key players in diosgenin-induced cardioprotective mechanisms.</description><subject>Animals</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Arrhythmias, Cardiac - drug therapy</subject><subject>Arrhythmias, Cardiac - metabolism</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Decanoic Acids - pharmacology</subject><subject>Diosgenin - pharmacology</subject><subject>Heart - drug effects</subject><subject>Hydroxy Acids - pharmacology</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Male</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide - metabolism</subject><subject>Original Paper</subject><subject>Potassium Channels - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Tachycardia, Ventricular - drug therapy</subject><subject>Tachycardia, Ventricular - metabolism</subject><subject>Ventricular Fibrillation - drug therapy</subject><subject>Ventricular Fibrillation - metabolism</subject><issn>1880-6546</issn><issn>1880-6562</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc9uFSEUhyfGxtbqA7gxLN2gMDAMuDE3jf9ik7qoa0Lh0KGZgSswjfMwfVdncuuNTUggOb_znUO-pnlDyXtKSP-h0LbrBSaUY8IYw_JZc0alJFh0on1-fHNx2rws5Y4QLlQrXzSnbUc7oiQ_ax52sQZsch6WOkzBIvAebEXJIxdSuYUYIlpPhj1kP5eQIg7RzRYcmpZkTXbBjGvibs7LFjQom4qm5GD8iIyt4d7UtWkDxlDzOiH9CQ5QWUqFCZm4ckJNdkjR5Q31Y3f9E9nBxAjjq-bEm7HA68f7vPn15fP1xTd8efX1-8XuElvWtxJ3UnhlO8kVpaKzzHjOPW17YZmwnbOWKAbrzzljHATxhjqrHCjuO8dvhGTnzacDdz_fTOAsxJrNqPc5TCYvOpmgn1ZiGPRtuteU9LQnLV0J7x4JOf2eoVQ9hWJhHE2ENBdNBVWMMiXFGqWHqM2plAz-OIcSvXnVB6969ao3r3pb8O3_Cx47_olkfwFy2qIj</recordid><startdate>201411</startdate><enddate>201411</enddate><creator>Badalzadeh, Reza</creator><creator>Yousefi, Bahman</creator><creator>Majidinia, Maryam</creator><creator>Ebrahimi, Hadi</creator><general>Springer Japan</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>201411</creationdate><title>Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial KATP channel</title><author>Badalzadeh, Reza ; Yousefi, Bahman ; Majidinia, Maryam ; Ebrahimi, Hadi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3728-586f9c58491165c3af44f1276c36c5dcc093e9284334e60fa1dc9de94f5d4b683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Arrhythmias, Cardiac - drug therapy</topic><topic>Arrhythmias, Cardiac - metabolism</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Decanoic Acids - pharmacology</topic><topic>Diosgenin - pharmacology</topic><topic>Heart - drug effects</topic><topic>Hydroxy Acids - pharmacology</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Male</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide - metabolism</topic><topic>Original Paper</topic><topic>Potassium Channels - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Tachycardia, Ventricular - drug therapy</topic><topic>Tachycardia, Ventricular - metabolism</topic><topic>Ventricular Fibrillation - drug therapy</topic><topic>Ventricular Fibrillation - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Badalzadeh, Reza</creatorcontrib><creatorcontrib>Yousefi, Bahman</creatorcontrib><creatorcontrib>Majidinia, Maryam</creatorcontrib><creatorcontrib>Ebrahimi, Hadi</creatorcontrib><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><collection>PubMed Central (Full Participant titles)</collection><jtitle>The journal of physiological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Badalzadeh, Reza</au><au>Yousefi, Bahman</au><au>Majidinia, Maryam</au><au>Ebrahimi, Hadi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial KATP channel</atitle><jtitle>The journal of physiological sciences</jtitle><addtitle>J Physiol Sci</addtitle><date>2014-11</date><risdate>2014</risdate><volume>64</volume><issue>6</issue><spage>393</spage><epage>400</epage><pages>393-400</pages><issn>1880-6546</issn><eissn>1880-6562</eissn><abstract>This study was designed to investigate the anti-arrhythmic effect of diosgenin preconditioning in myocardial reperfusion injury in rat, focusing on the involvement of the nitric oxide (NO) system and mitochondrial ATP-dependent potassium (mitoKATP) channels in this scenario. After isolation of the hearts of male Wister rats, the study was conducted in an isolated buffer-perfused heart model. Global ischemia (for 30 min) was induced by interruption of the aortic supply, which was followed by 90-min reperfusion. Throughout the experiment, the electrocardiograms of hearts were monitored using three golden surface electrodes connected to a data acquisition system. Arrhythmias were assessed based on the Lambeth convention and were categorized as number, duration and incidence of ventricular tachycardia (VT), ventricular fibrillation (VF), and premature ventricular complexes (PVC), and arrhythmic score. Additionally, lactate dehydrogenase (LDH) levels in coronary effluent were estimated colorimetrically. Diosgenin pre-administration for 20 min before ischemia reduced the LDH release into the coronary effluent, as compared with control hearts (P < 0.05). In addition, the diosgenin-receiving group showed a lower number of PVC, VT and VF, a reduced duration and incidence of VT and VF, and less severe arrhythmia at reperfusion phase, in comparison with controls. Blocking the mitoKATP channels using 5-hydroxydecanoate as well as inhibiting the NO system through prior administration of L-NAME significantly reduced the positive effects of diosgenin. Our finding showed that pre-administration of diosgenin could provide cardioprotection through anti-arrhythmic effects against ischemia-reperfusion (I/R) injury in isolated rat hearts. In addition, mitoKATP channels and NO system may be the key players in diosgenin-induced cardioprotective mechanisms.</abstract><cop>Japan</cop><pub>Springer Japan</pub><pmid>25150984</pmid><doi>10.1007/s12576-014-0333-8</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Arrhythmia Agents - pharmacology Arrhythmias, Cardiac - drug therapy Arrhythmias, Cardiac - metabolism Cardiotonic Agents - pharmacology Decanoic Acids - pharmacology Diosgenin - pharmacology Heart - drug effects Hydroxy Acids - pharmacology L-Lactate Dehydrogenase - metabolism Male Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - metabolism NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - metabolism Original Paper Potassium Channels - metabolism Rats Rats, Wistar Tachycardia, Ventricular - drug therapy Tachycardia, Ventricular - metabolism Ventricular Fibrillation - drug therapy Ventricular Fibrillation - metabolism |
| title | Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial KATP channel |
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