Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms
The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF coul...
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Veröffentlicht in: | Journal of electrocardiology 1995, Vol.28 Suppl, p.21-24 |
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description | The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF could potentially mediate the time-dependent effects of VF duration on defibrillation. Defibrillation threshold (DFT) was therefore determined in dogs during concurrent infusion of adenosine and dipyridamole (a nucleoside transport blocker). Transthoracic DFT increased by approximately 50%, whereas transmyocardial DFT increased by approximately 100% in a separate group of dogs. These effects of adenosine on DFT were abolished when the dogs were autonomically denervated, suggesting that the deleterious effects of adenosine on DFT are due to its antiadrenergic mechanism of action. These data indicate that adenosine release during VF can markedly increase DFT. Since adenosine myocardial release during VF is time dependent, it is likely that adenosine plays a significant role in mediating the increase in threshold that is dependent on the duration of VF. |
doi_str_mv | 10.1016/S0022-0736(95)80004-2 |
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Potential mechanisms</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Lerman, B B ; Engelstein, E D</creator><creatorcontrib>Lerman, B B ; Engelstein, E D</creatorcontrib><description>The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF could potentially mediate the time-dependent effects of VF duration on defibrillation. Defibrillation threshold (DFT) was therefore determined in dogs during concurrent infusion of adenosine and dipyridamole (a nucleoside transport blocker). Transthoracic DFT increased by approximately 50%, whereas transmyocardial DFT increased by approximately 100% in a separate group of dogs. These effects of adenosine on DFT were abolished when the dogs were autonomically denervated, suggesting that the deleterious effects of adenosine on DFT are due to its antiadrenergic mechanism of action. These data indicate that adenosine release during VF can markedly increase DFT. Since adenosine myocardial release during VF is time dependent, it is likely that adenosine plays a significant role in mediating the increase in threshold that is dependent on the duration of VF.</description><identifier>ISSN: 0022-0736</identifier><identifier>DOI: 10.1016/S0022-0736(95)80004-2</identifier><identifier>PMID: 8656114</identifier><language>eng</language><publisher>United States</publisher><subject>Adenosine - antagonists & inhibitors ; Adenosine - metabolism ; Adenosine - pharmacology ; Adenosine - physiology ; Adrenergic Antagonists - pharmacology ; Animals ; Autonomic Nervous System - physiopathology ; Cardiovascular Agents - pharmacology ; Denervation ; Dipyridamole - pharmacology ; Dogs ; Electric Countershock ; Epinephrine - metabolism ; Lactates - metabolism ; Myocardium - metabolism ; Norepinephrine - metabolism ; Nucleosides - antagonists & inhibitors ; Time Factors ; Vagotomy ; Ventricular Fibrillation - metabolism ; Ventricular Fibrillation - physiopathology ; Ventricular Fibrillation - therapy</subject><ispartof>Journal of electrocardiology, 1995, Vol.28 Suppl, p.21-24</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27902,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8656114$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lerman, B B</creatorcontrib><creatorcontrib>Engelstein, E D</creatorcontrib><title>Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms</title><title>Journal of electrocardiology</title><addtitle>J Electrocardiol</addtitle><description>The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF could potentially mediate the time-dependent effects of VF duration on defibrillation. Defibrillation threshold (DFT) was therefore determined in dogs during concurrent infusion of adenosine and dipyridamole (a nucleoside transport blocker). Transthoracic DFT increased by approximately 50%, whereas transmyocardial DFT increased by approximately 100% in a separate group of dogs. These effects of adenosine on DFT were abolished when the dogs were autonomically denervated, suggesting that the deleterious effects of adenosine on DFT are due to its antiadrenergic mechanism of action. These data indicate that adenosine release during VF can markedly increase DFT. Since adenosine myocardial release during VF is time dependent, it is likely that adenosine plays a significant role in mediating the increase in threshold that is dependent on the duration of VF.</description><subject>Adenosine - antagonists & inhibitors</subject><subject>Adenosine - metabolism</subject><subject>Adenosine - pharmacology</subject><subject>Adenosine - physiology</subject><subject>Adrenergic Antagonists - pharmacology</subject><subject>Animals</subject><subject>Autonomic Nervous System - physiopathology</subject><subject>Cardiovascular Agents - pharmacology</subject><subject>Denervation</subject><subject>Dipyridamole - pharmacology</subject><subject>Dogs</subject><subject>Electric Countershock</subject><subject>Epinephrine - metabolism</subject><subject>Lactates - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Norepinephrine - metabolism</subject><subject>Nucleosides - antagonists & inhibitors</subject><subject>Time Factors</subject><subject>Vagotomy</subject><subject>Ventricular Fibrillation - metabolism</subject><subject>Ventricular Fibrillation - physiopathology</subject><subject>Ventricular Fibrillation - therapy</subject><issn>0022-0736</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpV0E1LAzEQBuAclFqrP6GQk-hh6ySbZJOjFKuFgoJ6XvK1NLIfNckK_nsXLYKnGd55GIZBaElgRYCI2xcASguoSnGt-I0EAFbQEzT_i8_QeUrvU65oRWdoJgUXhLA50tveRq-Td9j5JpgY2lbnMPQ476NP-6GdBqPHecCfvs8x2LHVEf-Tbow_zQo_D3lCQbe483av-5C6dIFOG90mf3msC_S2uX9dPxa7p4ft-m5XHCiIXCgODAyVxlvFJRUeCGWWl1o2jpSiUrJpjNWWGcuBgrIUNHOKCyPLSgpXLtDV795DHD5Gn3LdhWT9dGTvhzHV1aRAcDbB5RGOpvOuPsTQ6fhVH39SfgOhBmQi</recordid><startdate>1995</startdate><enddate>1995</enddate><creator>Lerman, B B</creator><creator>Engelstein, E D</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>1995</creationdate><title>Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms</title><author>Lerman, B B ; Engelstein, E D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p206t-95040b28bec95826e0124c53a8fd136798ffbcac4bc50209c20a4d956b83786d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Adenosine - antagonists & inhibitors</topic><topic>Adenosine - metabolism</topic><topic>Adenosine - pharmacology</topic><topic>Adenosine - physiology</topic><topic>Adrenergic Antagonists - pharmacology</topic><topic>Animals</topic><topic>Autonomic Nervous System - physiopathology</topic><topic>Cardiovascular Agents - pharmacology</topic><topic>Denervation</topic><topic>Dipyridamole - pharmacology</topic><topic>Dogs</topic><topic>Electric Countershock</topic><topic>Epinephrine - metabolism</topic><topic>Lactates - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Norepinephrine - metabolism</topic><topic>Nucleosides - antagonists & inhibitors</topic><topic>Time Factors</topic><topic>Vagotomy</topic><topic>Ventricular Fibrillation - metabolism</topic><topic>Ventricular Fibrillation - physiopathology</topic><topic>Ventricular Fibrillation - therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lerman, B B</creatorcontrib><creatorcontrib>Engelstein, E D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of electrocardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lerman, B B</au><au>Engelstein, E D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms</atitle><jtitle>Journal of electrocardiology</jtitle><addtitle>J Electrocardiol</addtitle><date>1995</date><risdate>1995</risdate><volume>28 Suppl</volume><spage>21</spage><epage>24</epage><pages>21-24</pages><issn>0022-0736</issn><abstract>The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF could potentially mediate the time-dependent effects of VF duration on defibrillation. Defibrillation threshold (DFT) was therefore determined in dogs during concurrent infusion of adenosine and dipyridamole (a nucleoside transport blocker). Transthoracic DFT increased by approximately 50%, whereas transmyocardial DFT increased by approximately 100% in a separate group of dogs. These effects of adenosine on DFT were abolished when the dogs were autonomically denervated, suggesting that the deleterious effects of adenosine on DFT are due to its antiadrenergic mechanism of action. These data indicate that adenosine release during VF can markedly increase DFT. Since adenosine myocardial release during VF is time dependent, it is likely that adenosine plays a significant role in mediating the increase in threshold that is dependent on the duration of VF.</abstract><cop>United States</cop><pmid>8656114</pmid><doi>10.1016/S0022-0736(95)80004-2</doi><tpages>4</tpages></addata></record> |
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subjects | Adenosine - antagonists & inhibitors Adenosine - metabolism Adenosine - pharmacology Adenosine - physiology Adrenergic Antagonists - pharmacology Animals Autonomic Nervous System - physiopathology Cardiovascular Agents - pharmacology Denervation Dipyridamole - pharmacology Dogs Electric Countershock Epinephrine - metabolism Lactates - metabolism Myocardium - metabolism Norepinephrine - metabolism Nucleosides - antagonists & inhibitors Time Factors Vagotomy Ventricular Fibrillation - metabolism Ventricular Fibrillation - physiopathology Ventricular Fibrillation - therapy |
title | Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms |
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