Biphasic Response of Action Potential Duration to Sudden Sympathetic Stimulation in Anesthetized Cats
Although certain roles of the sympathetic nervous system have been suggested as possible mechanisms of life-threatening arrhythmias and sudden cardiac death, the dynamic electrophysiological response to sympathetic activation remains unclear. The aim of this study was to investigate the dynamic resp...
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Veröffentlicht in: | Circulation Journal 2003, Vol.67(10), pp.876-880 |
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container_title | Circulation Journal |
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description | Although certain roles of the sympathetic nervous system have been suggested as possible mechanisms of life-threatening arrhythmias and sudden cardiac death, the dynamic electrophysiological response to sympathetic activation remains unclear. The aim of this study was to investigate the dynamic response of action potential duration (APD) to sudden sympathetic stimulation (SYM) using monophasic action potential (MAP) recording. In 10 anesthetized cats, MAPs were continuously recorded from the right ventricular endocardium under constant pacing. The dynamic response of the APD to SYM (3 Hz) were examined before and after the administration of propranolol (0.5 mg/kg iv) (n=5) or phentolamine (1.0 mg/kg iv) (n=5). In response to SYM, the APD was transiently prolonged by 5.5±3.2 ms at 7.0±1.3 s, and monotonically shortened toward a steady-state level (-14.5±6.9 ms). Propranolol almost abolished both the transient prolongation (6.6±4.5 to 0.2±0.4 ms, p |
doi_str_mv | 10.1253/circj.67.876 |
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The aim of this study was to investigate the dynamic response of action potential duration (APD) to sudden sympathetic stimulation (SYM) using monophasic action potential (MAP) recording. In 10 anesthetized cats, MAPs were continuously recorded from the right ventricular endocardium under constant pacing. The dynamic response of the APD to SYM (3 Hz) were examined before and after the administration of propranolol (0.5 mg/kg iv) (n=5) or phentolamine (1.0 mg/kg iv) (n=5). In response to SYM, the APD was transiently prolonged by 5.5±3.2 ms at 7.0±1.3 s, and monotonically shortened toward a steady-state level (-14.5±6.9 ms). Propranolol almost abolished both the transient prolongation (6.6±4.5 to 0.2±0.4 ms, p<0.05) and the steady-state shortening (-13.7±3.6 to -1.1±2.4 ms, p<0.005), whereas phentolamine did not have a significant effect on the response of APD to SYM. These findings might partly account for the propensity of ventricular arrhythmias to occur immediately after sudden sympathetic activation. (Circ J 2003; 67: 876 - 880)</description><identifier>ISSN: 1346-9843</identifier><identifier>EISSN: 1347-4820</identifier><identifier>DOI: 10.1253/circj.67.876</identifier><identifier>PMID: 14578623</identifier><language>eng</language><publisher>Kyoto: The Japanese Circulation Society</publisher><subject>Action potential duration ; Action Potentials - drug effects ; Action Potentials - physiology ; Adrenergic alpha-Antagonists - pharmacology ; Anesthesia ; Animals ; Autonomic nervous system ; Biological and medical sciences ; Cardiac dysrhythmias ; Cardiac Pacing, Artificial ; Cardiology. Vascular system ; Cats ; Electrophysiology ; Heart ; Medical sciences ; Phentolamine - pharmacology ; Propranolol - pharmacology ; Sympathetic Nervous System - drug effects ; Sympathetic Nervous System - physiology ; Ventricular arrhythmias ; Ventricular Fibrillation - etiology ; Ventricular Function</subject><ispartof>Circulation Journal, 2003, Vol.67(10), pp.876-880</ispartof><rights>2003 THE JAPANESE CIRCULATION SOCIETY</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c606t-a9b5e41c14a30bfcc0594eb03198303ab2d81b2963a0b3f8f64bce23d6658cf83</citedby><cites>FETCH-LOGICAL-c606t-a9b5e41c14a30bfcc0594eb03198303ab2d81b2963a0b3f8f64bce23d6658cf83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15266080$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14578623$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tatewaki, Teiji</creatorcontrib><creatorcontrib>Inagaki, Masashi</creatorcontrib><creatorcontrib>Kawada, Toru</creatorcontrib><creatorcontrib>Shishido, Toshiaki</creatorcontrib><creatorcontrib>Yanagiya, Yusuke</creatorcontrib><creatorcontrib>Takaki, Hiroshi</creatorcontrib><creatorcontrib>Sato, Takayuki</creatorcontrib><creatorcontrib>Sugimachi, Masaru</creatorcontrib><creatorcontrib>Sunagawa, Kenji</creatorcontrib><title>Biphasic Response of Action Potential Duration to Sudden Sympathetic Stimulation in Anesthetized Cats</title><title>Circulation Journal</title><addtitle>Circ J</addtitle><description>Although certain roles of the sympathetic nervous system have been suggested as possible mechanisms of life-threatening arrhythmias and sudden cardiac death, the dynamic electrophysiological response to sympathetic activation remains unclear. The aim of this study was to investigate the dynamic response of action potential duration (APD) to sudden sympathetic stimulation (SYM) using monophasic action potential (MAP) recording. In 10 anesthetized cats, MAPs were continuously recorded from the right ventricular endocardium under constant pacing. The dynamic response of the APD to SYM (3 Hz) were examined before and after the administration of propranolol (0.5 mg/kg iv) (n=5) or phentolamine (1.0 mg/kg iv) (n=5). In response to SYM, the APD was transiently prolonged by 5.5±3.2 ms at 7.0±1.3 s, and monotonically shortened toward a steady-state level (-14.5±6.9 ms). Propranolol almost abolished both the transient prolongation (6.6±4.5 to 0.2±0.4 ms, p<0.05) and the steady-state shortening (-13.7±3.6 to -1.1±2.4 ms, p<0.005), whereas phentolamine did not have a significant effect on the response of APD to SYM. These findings might partly account for the propensity of ventricular arrhythmias to occur immediately after sudden sympathetic activation. (Circ J 2003; 67: 876 - 880)</description><subject>Action potential duration</subject><subject>Action Potentials - drug effects</subject><subject>Action Potentials - physiology</subject><subject>Adrenergic alpha-Antagonists - pharmacology</subject><subject>Anesthesia</subject><subject>Animals</subject><subject>Autonomic nervous system</subject><subject>Biological and medical sciences</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiac Pacing, Artificial</subject><subject>Cardiology. Vascular system</subject><subject>Cats</subject><subject>Electrophysiology</subject><subject>Heart</subject><subject>Medical sciences</subject><subject>Phentolamine - pharmacology</subject><subject>Propranolol - pharmacology</subject><subject>Sympathetic Nervous System - drug effects</subject><subject>Sympathetic Nervous System - physiology</subject><subject>Ventricular arrhythmias</subject><subject>Ventricular Fibrillation - etiology</subject><subject>Ventricular Function</subject><issn>1346-9843</issn><issn>1347-4820</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkM-v1CAQx4nR-H7ozbPhoie7QmmBHvetPjV5icbVM5nSqcumpRXo4fnXi9uNewEy82Hmmw8hrzjb8LIW760L9riRaqOVfEKuuahUUemSPT29ZdHoSlyRmxiPjJUNq5vn5IpXtdKyFNcE79x8gOgs_Y5xnnxEOvV0a5ObPP02JfTJwUA_LAFOpTTR_dJ16On-cZwhHTDlv_vkxmVYCefp1mM8df5gR3eQ4gvyrIch4svzfUt-3n_8sftcPHz99GW3fSisZDIV0LQ1VtzyCgRre2tz2gpbJnijBRPQlp3mbdlIAawVve5l1VosRSdlrW2vxS15u86dw_R7ySHM6KLFYQCP0xKN4oKpRqkMvltBG6YYA_ZmDm6E8Gg4M_-0mpNWI5XJWjP--jx3aUfsLvDZYwbenAGIFoY-gLcuXri6lJJplrndyh1jgl_4H4CQNQ542ZpjrGdef-keIBj04i9wq5pY</recordid><startdate>2003</startdate><enddate>2003</enddate><creator>Tatewaki, Teiji</creator><creator>Inagaki, Masashi</creator><creator>Kawada, Toru</creator><creator>Shishido, Toshiaki</creator><creator>Yanagiya, Yusuke</creator><creator>Takaki, Hiroshi</creator><creator>Sato, Takayuki</creator><creator>Sugimachi, Masaru</creator><creator>Sunagawa, Kenji</creator><general>The Japanese Circulation Society</general><general>Japanese Circulation Society</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>2003</creationdate><title>Biphasic Response of Action Potential Duration to Sudden Sympathetic Stimulation in Anesthetized Cats</title><author>Tatewaki, Teiji ; Inagaki, Masashi ; Kawada, Toru ; Shishido, Toshiaki ; Yanagiya, Yusuke ; Takaki, Hiroshi ; Sato, Takayuki ; Sugimachi, Masaru ; Sunagawa, Kenji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c606t-a9b5e41c14a30bfcc0594eb03198303ab2d81b2963a0b3f8f64bce23d6658cf83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Action potential duration</topic><topic>Action Potentials - drug effects</topic><topic>Action Potentials - physiology</topic><topic>Adrenergic alpha-Antagonists - pharmacology</topic><topic>Anesthesia</topic><topic>Animals</topic><topic>Autonomic nervous system</topic><topic>Biological and medical sciences</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiac Pacing, Artificial</topic><topic>Cardiology. Vascular system</topic><topic>Cats</topic><topic>Electrophysiology</topic><topic>Heart</topic><topic>Medical sciences</topic><topic>Phentolamine - pharmacology</topic><topic>Propranolol - pharmacology</topic><topic>Sympathetic Nervous System - drug effects</topic><topic>Sympathetic Nervous System - physiology</topic><topic>Ventricular arrhythmias</topic><topic>Ventricular Fibrillation - etiology</topic><topic>Ventricular Function</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tatewaki, Teiji</creatorcontrib><creatorcontrib>Inagaki, Masashi</creatorcontrib><creatorcontrib>Kawada, Toru</creatorcontrib><creatorcontrib>Shishido, Toshiaki</creatorcontrib><creatorcontrib>Yanagiya, Yusuke</creatorcontrib><creatorcontrib>Takaki, Hiroshi</creatorcontrib><creatorcontrib>Sato, Takayuki</creatorcontrib><creatorcontrib>Sugimachi, Masaru</creatorcontrib><creatorcontrib>Sunagawa, Kenji</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>Circulation Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tatewaki, Teiji</au><au>Inagaki, Masashi</au><au>Kawada, Toru</au><au>Shishido, Toshiaki</au><au>Yanagiya, Yusuke</au><au>Takaki, Hiroshi</au><au>Sato, Takayuki</au><au>Sugimachi, Masaru</au><au>Sunagawa, Kenji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biphasic Response of Action Potential Duration to Sudden Sympathetic Stimulation in Anesthetized Cats</atitle><jtitle>Circulation Journal</jtitle><addtitle>Circ J</addtitle><date>2003</date><risdate>2003</risdate><volume>67</volume><issue>10</issue><spage>876</spage><epage>880</epage><pages>876-880</pages><issn>1346-9843</issn><eissn>1347-4820</eissn><abstract>Although certain roles of the sympathetic nervous system have been suggested as possible mechanisms of life-threatening arrhythmias and sudden cardiac death, the dynamic electrophysiological response to sympathetic activation remains unclear. The aim of this study was to investigate the dynamic response of action potential duration (APD) to sudden sympathetic stimulation (SYM) using monophasic action potential (MAP) recording. In 10 anesthetized cats, MAPs were continuously recorded from the right ventricular endocardium under constant pacing. The dynamic response of the APD to SYM (3 Hz) were examined before and after the administration of propranolol (0.5 mg/kg iv) (n=5) or phentolamine (1.0 mg/kg iv) (n=5). In response to SYM, the APD was transiently prolonged by 5.5±3.2 ms at 7.0±1.3 s, and monotonically shortened toward a steady-state level (-14.5±6.9 ms). Propranolol almost abolished both the transient prolongation (6.6±4.5 to 0.2±0.4 ms, p<0.05) and the steady-state shortening (-13.7±3.6 to -1.1±2.4 ms, p<0.005), whereas phentolamine did not have a significant effect on the response of APD to SYM. These findings might partly account for the propensity of ventricular arrhythmias to occur immediately after sudden sympathetic activation. (Circ J 2003; 67: 876 - 880)</abstract><cop>Kyoto</cop><pub>The Japanese Circulation Society</pub><pmid>14578623</pmid><doi>10.1253/circj.67.876</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Action potential duration Action Potentials - drug effects Action Potentials - physiology Adrenergic alpha-Antagonists - pharmacology Anesthesia Animals Autonomic nervous system Biological and medical sciences Cardiac dysrhythmias Cardiac Pacing, Artificial Cardiology. Vascular system Cats Electrophysiology Heart Medical sciences Phentolamine - pharmacology Propranolol - pharmacology Sympathetic Nervous System - drug effects Sympathetic Nervous System - physiology Ventricular arrhythmias Ventricular Fibrillation - etiology Ventricular Function |
title | Biphasic Response of Action Potential Duration to Sudden Sympathetic Stimulation in Anesthetized Cats |
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