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Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs
Departments of 1 Biomedical Engineering, 2 Medicine, and 3 Physiology, University of Alabama at Birmingham, Birmingham, Alabama Submitted 5 May 2008 ; accepted in final form 23 June 2008 Endocardial mapping has suggested that Purkinje fibers may play a role in the maintenance of long-duration ventri...
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Published in: | American journal of physiology. Heart and circulatory physiology 2008-08, Vol.295 (2), p.H883-H889 |
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container_title | American journal of physiology. Heart and circulatory physiology |
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creator | Dosdall, Derek J Tabereaux, Paul B Kim, Jong J Walcott, Gregory P Rogers, Jack M Killingsworth, Cheryl R Huang, Jian Robertson, Peter G Smith, William M Ideker, Raymond E |
description | Departments of 1 Biomedical Engineering, 2 Medicine, and 3 Physiology, University of Alabama at Birmingham, Birmingham, Alabama
Submitted 5 May 2008
; accepted in final form 23 June 2008
Endocardial mapping has suggested that Purkinje fibers may play a role in the maintenance of long-duration ventricular fibrillation (LDVF). To determine the influence of Purkinje fibers on LDVF, we chemically ablated the Purkinje system with Lugol solution and recorded endocardial and transmural activation during LDVF. Dog hearts were isolated and perfused, and the ventricular endocardium was exposed and treated with Lugol solution ( n = 6) or normal Tyrode solution as a control ( n = 6). The left anterior papillary muscle endocardium was mapped with a 504-electrode (21 x 24) plaque with electrodes spaced 1 mm apart. Transmural activation was recorded with a six-electrode plunge needle on each side of the plaque. Ventricular fibrillation (VF) was induced, and perfusion was halted. LDVF spontaneously terminated sooner in Lugol-ablated hearts than in control hearts (4.9 ± 1.5 vs. 9.2 ± 3.2 min, P = 0.01). After termination of VF, both the control and Lugol hearts were typically excitable, but only short episodes of VF could be reinduced. Endocardial activation rates were similar during the first 2 min of LDVF for Lugol-ablated and control hearts but were significantly slower in Lugol hearts by 3 min. In control hearts, the endocardium activated more rapidly than the epicardium after 4 min of LDVF with wave fronts propagating most often from the endocardium to epicardium. No difference in transmural activation rate or wave front direction was observed in Lugol hearts. Ablation of the subendocardium hastens VF spontaneous termination and alters VF activation sequences, suggesting that Purkinje fibers are important in the maintenance of LDVF.
electrophysiology; mapping; Lugol ablation; activation rate gradient
Address for reprint requests and other correspondence: R. E. Ideker, Volker Hall B140, 1670 Univ. Blvd., Birmingham, AL 35294-0019 (e-mail: rei{at}crml.uab.edu ) |
doi_str_mv | 10.1152/ajpheart.00466.2008 |
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Submitted 5 May 2008
; accepted in final form 23 June 2008
Endocardial mapping has suggested that Purkinje fibers may play a role in the maintenance of long-duration ventricular fibrillation (LDVF). To determine the influence of Purkinje fibers on LDVF, we chemically ablated the Purkinje system with Lugol solution and recorded endocardial and transmural activation during LDVF. Dog hearts were isolated and perfused, and the ventricular endocardium was exposed and treated with Lugol solution ( n = 6) or normal Tyrode solution as a control ( n = 6). The left anterior papillary muscle endocardium was mapped with a 504-electrode (21 x 24) plaque with electrodes spaced 1 mm apart. Transmural activation was recorded with a six-electrode plunge needle on each side of the plaque. Ventricular fibrillation (VF) was induced, and perfusion was halted. LDVF spontaneously terminated sooner in Lugol-ablated hearts than in control hearts (4.9 ± 1.5 vs. 9.2 ± 3.2 min, P = 0.01). After termination of VF, both the control and Lugol hearts were typically excitable, but only short episodes of VF could be reinduced. Endocardial activation rates were similar during the first 2 min of LDVF for Lugol-ablated and control hearts but were significantly slower in Lugol hearts by 3 min. In control hearts, the endocardium activated more rapidly than the epicardium after 4 min of LDVF with wave fronts propagating most often from the endocardium to epicardium. No difference in transmural activation rate or wave front direction was observed in Lugol hearts. Ablation of the subendocardium hastens VF spontaneous termination and alters VF activation sequences, suggesting that Purkinje fibers are important in the maintenance of LDVF.
electrophysiology; mapping; Lugol ablation; activation rate gradient
Address for reprint requests and other correspondence: R. E. Ideker, Volker Hall B140, 1670 Univ. Blvd., Birmingham, AL 35294-0019 (e-mail: rei{at}crml.uab.edu )</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.00466.2008</identifier><identifier>PMID: 18586887</identifier><identifier>CODEN: AJPPDI</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Action Potentials ; Animals ; Body Surface Potential Mapping ; Cardiac Pacing, Artificial ; Cardiovascular system ; Cells ; Disease Models, Animal ; Dogs ; Electrodes ; Endocardium - drug effects ; Endocardium - physiopathology ; Heart ; In Vitro Techniques ; Iodides - pharmacology ; Purkinje Fibers - drug effects ; Purkinje Fibers - physiopathology ; Time Factors ; Ventricular Fibrillation - physiopathology</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2008-08, Vol.295 (2), p.H883-H889</ispartof><rights>Copyright American Physiological Society Aug 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c531t-681f3c4a07189b9f9ddfe85b4fb057082d20069b1c626e31fb8c289167997a473</citedby><cites>FETCH-LOGICAL-c531t-681f3c4a07189b9f9ddfe85b4fb057082d20069b1c626e31fb8c289167997a473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18586887$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dosdall, Derek J</creatorcontrib><creatorcontrib>Tabereaux, Paul B</creatorcontrib><creatorcontrib>Kim, Jong J</creatorcontrib><creatorcontrib>Walcott, Gregory P</creatorcontrib><creatorcontrib>Rogers, Jack M</creatorcontrib><creatorcontrib>Killingsworth, Cheryl R</creatorcontrib><creatorcontrib>Huang, Jian</creatorcontrib><creatorcontrib>Robertson, Peter G</creatorcontrib><creatorcontrib>Smith, William M</creatorcontrib><creatorcontrib>Ideker, Raymond E</creatorcontrib><title>Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Departments of 1 Biomedical Engineering, 2 Medicine, and 3 Physiology, University of Alabama at Birmingham, Birmingham, Alabama
Submitted 5 May 2008
; accepted in final form 23 June 2008
Endocardial mapping has suggested that Purkinje fibers may play a role in the maintenance of long-duration ventricular fibrillation (LDVF). To determine the influence of Purkinje fibers on LDVF, we chemically ablated the Purkinje system with Lugol solution and recorded endocardial and transmural activation during LDVF. Dog hearts were isolated and perfused, and the ventricular endocardium was exposed and treated with Lugol solution ( n = 6) or normal Tyrode solution as a control ( n = 6). The left anterior papillary muscle endocardium was mapped with a 504-electrode (21 x 24) plaque with electrodes spaced 1 mm apart. Transmural activation was recorded with a six-electrode plunge needle on each side of the plaque. Ventricular fibrillation (VF) was induced, and perfusion was halted. LDVF spontaneously terminated sooner in Lugol-ablated hearts than in control hearts (4.9 ± 1.5 vs. 9.2 ± 3.2 min, P = 0.01). After termination of VF, both the control and Lugol hearts were typically excitable, but only short episodes of VF could be reinduced. Endocardial activation rates were similar during the first 2 min of LDVF for Lugol-ablated and control hearts but were significantly slower in Lugol hearts by 3 min. In control hearts, the endocardium activated more rapidly than the epicardium after 4 min of LDVF with wave fronts propagating most often from the endocardium to epicardium. No difference in transmural activation rate or wave front direction was observed in Lugol hearts. Ablation of the subendocardium hastens VF spontaneous termination and alters VF activation sequences, suggesting that Purkinje fibers are important in the maintenance of LDVF.
electrophysiology; mapping; Lugol ablation; activation rate gradient
Address for reprint requests and other correspondence: R. E. Ideker, Volker Hall B140, 1670 Univ. Blvd., Birmingham, AL 35294-0019 (e-mail: rei{at}crml.uab.edu )</description><subject>Action Potentials</subject><subject>Animals</subject><subject>Body Surface Potential Mapping</subject><subject>Cardiac Pacing, Artificial</subject><subject>Cardiovascular system</subject><subject>Cells</subject><subject>Disease Models, Animal</subject><subject>Dogs</subject><subject>Electrodes</subject><subject>Endocardium - drug effects</subject><subject>Endocardium - physiopathology</subject><subject>Heart</subject><subject>In Vitro Techniques</subject><subject>Iodides - pharmacology</subject><subject>Purkinje Fibers - drug effects</subject><subject>Purkinje Fibers - physiopathology</subject><subject>Time Factors</subject><subject>Ventricular Fibrillation - physiopathology</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNp1kc1u1DAUhS0EokPLEyAhi30G_0wcmx0aUYpUiS7K2nISO_HgxMF2WvIUvDKeZmBWXVnWPd85uvcA8A6jLcYl-agOU69VSFuEdoxtCUL8BdjkCSlwScVLsEGU0YJhWl6ANzEeEEJlxehrcIF5yRnn1Qb82fd6sI1yUNVOJetH6A1MvYZ3c_hpx4OGcYlJD7BRc9QR5kS3wKTDYMdVr8YWqibZh_UbVMqM84927I5ezo9d0c5hnT7oMQXbzE4FaGwdrDul2hG2votX4JVRLuq3p_cS_Lj-cr-_KW6_f_22_3xbNCXFqWAcG9rsFKowF7Uwom2N5mW9M3XeEXHS5nMwUeOGEaYpNjVvCBeYVUJUalfRS_Bh9Z2C_zXrmOTBz2HMkZIQwcpKMJZFdBU1wccYtJFTsIMKi8RIHjuQ_zqQTx3IYweZen-ynutBt2fmdPQs2K6C3nb9ow1aTv0SrXe-W86ORJSSyBvOaQY-PQ9cz87d69_pP3kG5dQa-hewNK2k</recordid><startdate>20080801</startdate><enddate>20080801</enddate><creator>Dosdall, Derek J</creator><creator>Tabereaux, Paul B</creator><creator>Kim, Jong J</creator><creator>Walcott, Gregory P</creator><creator>Rogers, Jack M</creator><creator>Killingsworth, Cheryl R</creator><creator>Huang, Jian</creator><creator>Robertson, Peter G</creator><creator>Smith, William M</creator><creator>Ideker, Raymond E</creator><general>American Physiological Society</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>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20080801</creationdate><title>Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs</title><author>Dosdall, Derek J ; Tabereaux, Paul B ; Kim, Jong J ; Walcott, Gregory P ; Rogers, Jack M ; Killingsworth, Cheryl R ; Huang, Jian ; Robertson, Peter G ; Smith, William M ; Ideker, Raymond E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c531t-681f3c4a07189b9f9ddfe85b4fb057082d20069b1c626e31fb8c289167997a473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Action Potentials</topic><topic>Animals</topic><topic>Body Surface Potential Mapping</topic><topic>Cardiac Pacing, Artificial</topic><topic>Cardiovascular system</topic><topic>Cells</topic><topic>Disease Models, Animal</topic><topic>Dogs</topic><topic>Electrodes</topic><topic>Endocardium - drug effects</topic><topic>Endocardium - physiopathology</topic><topic>Heart</topic><topic>In Vitro Techniques</topic><topic>Iodides - pharmacology</topic><topic>Purkinje Fibers - drug effects</topic><topic>Purkinje Fibers - physiopathology</topic><topic>Time Factors</topic><topic>Ventricular Fibrillation - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dosdall, Derek J</creatorcontrib><creatorcontrib>Tabereaux, Paul B</creatorcontrib><creatorcontrib>Kim, Jong J</creatorcontrib><creatorcontrib>Walcott, Gregory P</creatorcontrib><creatorcontrib>Rogers, Jack M</creatorcontrib><creatorcontrib>Killingsworth, Cheryl R</creatorcontrib><creatorcontrib>Huang, Jian</creatorcontrib><creatorcontrib>Robertson, Peter G</creatorcontrib><creatorcontrib>Smith, William M</creatorcontrib><creatorcontrib>Ideker, Raymond E</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dosdall, Derek J</au><au>Tabereaux, Paul B</au><au>Kim, Jong J</au><au>Walcott, Gregory P</au><au>Rogers, Jack M</au><au>Killingsworth, Cheryl R</au><au>Huang, Jian</au><au>Robertson, Peter G</au><au>Smith, William M</au><au>Ideker, Raymond E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2008-08-01</date><risdate>2008</risdate><volume>295</volume><issue>2</issue><spage>H883</spage><epage>H889</epage><pages>H883-H889</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><coden>AJPPDI</coden><abstract>Departments of 1 Biomedical Engineering, 2 Medicine, and 3 Physiology, University of Alabama at Birmingham, Birmingham, Alabama
Submitted 5 May 2008
; accepted in final form 23 June 2008
Endocardial mapping has suggested that Purkinje fibers may play a role in the maintenance of long-duration ventricular fibrillation (LDVF). To determine the influence of Purkinje fibers on LDVF, we chemically ablated the Purkinje system with Lugol solution and recorded endocardial and transmural activation during LDVF. Dog hearts were isolated and perfused, and the ventricular endocardium was exposed and treated with Lugol solution ( n = 6) or normal Tyrode solution as a control ( n = 6). The left anterior papillary muscle endocardium was mapped with a 504-electrode (21 x 24) plaque with electrodes spaced 1 mm apart. Transmural activation was recorded with a six-electrode plunge needle on each side of the plaque. Ventricular fibrillation (VF) was induced, and perfusion was halted. LDVF spontaneously terminated sooner in Lugol-ablated hearts than in control hearts (4.9 ± 1.5 vs. 9.2 ± 3.2 min, P = 0.01). After termination of VF, both the control and Lugol hearts were typically excitable, but only short episodes of VF could be reinduced. Endocardial activation rates were similar during the first 2 min of LDVF for Lugol-ablated and control hearts but were significantly slower in Lugol hearts by 3 min. In control hearts, the endocardium activated more rapidly than the epicardium after 4 min of LDVF with wave fronts propagating most often from the endocardium to epicardium. No difference in transmural activation rate or wave front direction was observed in Lugol hearts. Ablation of the subendocardium hastens VF spontaneous termination and alters VF activation sequences, suggesting that Purkinje fibers are important in the maintenance of LDVF.
electrophysiology; mapping; Lugol ablation; activation rate gradient
Address for reprint requests and other correspondence: R. E. Ideker, Volker Hall B140, 1670 Univ. Blvd., Birmingham, AL 35294-0019 (e-mail: rei{at}crml.uab.edu )</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>18586887</pmid><doi>10.1152/ajpheart.00466.2008</doi><oa>free_for_read</oa></addata></record> |
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subjects | Action Potentials Animals Body Surface Potential Mapping Cardiac Pacing, Artificial Cardiovascular system Cells Disease Models, Animal Dogs Electrodes Endocardium - drug effects Endocardium - physiopathology Heart In Vitro Techniques Iodides - pharmacology Purkinje Fibers - drug effects Purkinje Fibers - physiopathology Time Factors Ventricular Fibrillation - physiopathology |
title | Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs |
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