The influence of cardiac cholinergic activation on the induction and maintenance of ventricular fibrillation
The influence of cardiac cholinergic activation was studied in rats and cats on the induction and maintenance of ventricular fibrillation (VF). Acetylcholine (ACH 2-25 micrograms/kg), in doses which did not cause bradycardia or hypotension, induced appearance of spontaneous VF (duration 2-60 sec.) i...
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Veröffentlicht in: | Basic research in cardiology 1984-11, Vol.79 (6), p.690-697 |
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description | The influence of cardiac cholinergic activation was studied in rats and cats on the induction and maintenance of ventricular fibrillation (VF). Acetylcholine (ACH 2-25 micrograms/kg), in doses which did not cause bradycardia or hypotension, induced appearance of spontaneous VF (duration 2-60 sec.) in 9/20 rats which have a high sympathetic autoregulation and in 3/6 cats only, 20-40 secs after the latter had been given adrenaline. ACh (10-45 micrograms/kg) and methacholine (10-40 micrograms/kg) also significantly prolonged the fibrillatory period induced electrically in cats and rats with and without atrial or ventricular pacing. The induction or prolongation of VF did not occur when higher doses of ACh (50-100 micrograms/kg) were given to rats. The influence of moderate amounts of cholinergic agents on the heart may be due to localised effects resulting in asynchronous activity. Alternatively, they may produce a discharge of multiple ectopic pacemakers or a disturbance in impulse conduction. Higher doses of ACh depress the S-A and ventricular ectopic activity node thereby decreasing the probability of inducing VF. It is concluded that under conditions of raised cardiac adrenergic activity, a moderate increase in cholinergic influence can both induce and prolong VF. The relevance of these findings to the "sudden infant death" syndrome is discussed. |
doi_str_mv | 10.1007/BF01908386 |
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Acetylcholine (ACH 2-25 micrograms/kg), in doses which did not cause bradycardia or hypotension, induced appearance of spontaneous VF (duration 2-60 sec.) in 9/20 rats which have a high sympathetic autoregulation and in 3/6 cats only, 20-40 secs after the latter had been given adrenaline. ACh (10-45 micrograms/kg) and methacholine (10-40 micrograms/kg) also significantly prolonged the fibrillatory period induced electrically in cats and rats with and without atrial or ventricular pacing. The induction or prolongation of VF did not occur when higher doses of ACh (50-100 micrograms/kg) were given to rats. The influence of moderate amounts of cholinergic agents on the heart may be due to localised effects resulting in asynchronous activity. Alternatively, they may produce a discharge of multiple ectopic pacemakers or a disturbance in impulse conduction. Higher doses of ACh depress the S-A and ventricular ectopic activity node thereby decreasing the probability of inducing VF. It is concluded that under conditions of raised cardiac adrenergic activity, a moderate increase in cholinergic influence can both induce and prolong VF. The relevance of these findings to the "sudden infant death" syndrome is discussed.</description><identifier>ISSN: 0300-8428</identifier><identifier>EISSN: 1435-1803</identifier><identifier>DOI: 10.1007/BF01908386</identifier><identifier>PMID: 6398060</identifier><identifier>CODEN: BRCAB7</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Acetylcholine - pharmacology ; Animals ; Biological and medical sciences ; Cardiac dysrhythmias ; Cardiology. Vascular system ; Cats ; Electric Stimulation ; Electrocardiography ; Female ; Heart ; Heart - drug effects ; Male ; Medical sciences ; Methacholine Chloride ; Methacholine Compounds - pharmacology ; Parasympathomimetics - pharmacology ; Rats ; Ventricular Fibrillation - etiology ; Ventricular Fibrillation - physiopathology</subject><ispartof>Basic research in cardiology, 1984-11, Vol.79 (6), p.690-697</ispartof><rights>1985 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8942509$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6398060$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>AMITZUR, G</creatorcontrib><creatorcontrib>MANOACH, M</creatorcontrib><creatorcontrib>WEINSTOCK, M</creatorcontrib><title>The influence of cardiac cholinergic activation on the induction and maintenance of ventricular fibrillation</title><title>Basic research in cardiology</title><addtitle>Basic Res Cardiol</addtitle><description>The influence of cardiac cholinergic activation was studied in rats and cats on the induction and maintenance of ventricular fibrillation (VF). Acetylcholine (ACH 2-25 micrograms/kg), in doses which did not cause bradycardia or hypotension, induced appearance of spontaneous VF (duration 2-60 sec.) in 9/20 rats which have a high sympathetic autoregulation and in 3/6 cats only, 20-40 secs after the latter had been given adrenaline. ACh (10-45 micrograms/kg) and methacholine (10-40 micrograms/kg) also significantly prolonged the fibrillatory period induced electrically in cats and rats with and without atrial or ventricular pacing. The induction or prolongation of VF did not occur when higher doses of ACh (50-100 micrograms/kg) were given to rats. The influence of moderate amounts of cholinergic agents on the heart may be due to localised effects resulting in asynchronous activity. Alternatively, they may produce a discharge of multiple ectopic pacemakers or a disturbance in impulse conduction. Higher doses of ACh depress the S-A and ventricular ectopic activity node thereby decreasing the probability of inducing VF. It is concluded that under conditions of raised cardiac adrenergic activity, a moderate increase in cholinergic influence can both induce and prolong VF. The relevance of these findings to the "sudden infant death" syndrome is discussed.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. Vascular system</subject><subject>Cats</subject><subject>Electric Stimulation</subject><subject>Electrocardiography</subject><subject>Female</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methacholine Chloride</subject><subject>Methacholine Compounds - pharmacology</subject><subject>Parasympathomimetics - pharmacology</subject><subject>Rats</subject><subject>Ventricular Fibrillation - etiology</subject><subject>Ventricular Fibrillation - physiopathology</subject><issn>0300-8428</issn><issn>1435-1803</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9UEtLAzEQDqLUWr14F3IQb6t5bZI9arEqFLzU85LNTmwkzdZkt-C_d6mLMDDMfA_mG4SuKbmnhKiHpxWhFdFcyxM0p4KXBdWEn6I54YQUWjB9ji5y_iKECinpDM0krzSRZI7CZgvYRxcGiBZw57A1qfXGYrvtgo-QPr3Fxvb-YHrfRTxWf5S0gz0uTGzxzvjYQzSTxQFin7wdgknY-Sb5EI7iS3TmTMhwNfUF-lg9b5avxfr95W35uC72VKq-UNow3jpOjaSsAsIYN5RKAM6okwqYUGMKpUpLxxksA3BNZaBxthXacb5Ad3---9R9D5D7euezhfGKCN2Qa1XqSmohRuLNRByaHbT1PvmdST_19J4Rv51wk60JLo0Jff6n6UqwklT8F7GCdIo</recordid><startdate>198411</startdate><enddate>198411</enddate><creator>AMITZUR, G</creator><creator>MANOACH, M</creator><creator>WEINSTOCK, M</creator><general>Springer</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>198411</creationdate><title>The influence of cardiac cholinergic activation on the induction and maintenance of ventricular fibrillation</title><author>AMITZUR, G ; MANOACH, M ; WEINSTOCK, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p167t-78a23df31a6129e0223a116ee321f67e247661775c11f6ec2eefb9aebfcd48f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiology. Vascular system</topic><topic>Cats</topic><topic>Electric Stimulation</topic><topic>Electrocardiography</topic><topic>Female</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methacholine Chloride</topic><topic>Methacholine Compounds - pharmacology</topic><topic>Parasympathomimetics - pharmacology</topic><topic>Rats</topic><topic>Ventricular Fibrillation - etiology</topic><topic>Ventricular Fibrillation - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>AMITZUR, G</creatorcontrib><creatorcontrib>MANOACH, M</creatorcontrib><creatorcontrib>WEINSTOCK, M</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>MEDLINE - Academic</collection><jtitle>Basic research in cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>AMITZUR, G</au><au>MANOACH, M</au><au>WEINSTOCK, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The influence of cardiac cholinergic activation on the induction and maintenance of ventricular fibrillation</atitle><jtitle>Basic research in cardiology</jtitle><addtitle>Basic Res Cardiol</addtitle><date>1984-11</date><risdate>1984</risdate><volume>79</volume><issue>6</issue><spage>690</spage><epage>697</epage><pages>690-697</pages><issn>0300-8428</issn><eissn>1435-1803</eissn><coden>BRCAB7</coden><abstract>The influence of cardiac cholinergic activation was studied in rats and cats on the induction and maintenance of ventricular fibrillation (VF). Acetylcholine (ACH 2-25 micrograms/kg), in doses which did not cause bradycardia or hypotension, induced appearance of spontaneous VF (duration 2-60 sec.) in 9/20 rats which have a high sympathetic autoregulation and in 3/6 cats only, 20-40 secs after the latter had been given adrenaline. ACh (10-45 micrograms/kg) and methacholine (10-40 micrograms/kg) also significantly prolonged the fibrillatory period induced electrically in cats and rats with and without atrial or ventricular pacing. The induction or prolongation of VF did not occur when higher doses of ACh (50-100 micrograms/kg) were given to rats. The influence of moderate amounts of cholinergic agents on the heart may be due to localised effects resulting in asynchronous activity. Alternatively, they may produce a discharge of multiple ectopic pacemakers or a disturbance in impulse conduction. Higher doses of ACh depress the S-A and ventricular ectopic activity node thereby decreasing the probability of inducing VF. It is concluded that under conditions of raised cardiac adrenergic activity, a moderate increase in cholinergic influence can both induce and prolong VF. The relevance of these findings to the "sudden infant death" syndrome is discussed.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>6398060</pmid><doi>10.1007/BF01908386</doi><tpages>8</tpages></addata></record> |
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subjects | Acetylcholine - pharmacology Animals Biological and medical sciences Cardiac dysrhythmias Cardiology. Vascular system Cats Electric Stimulation Electrocardiography Female Heart Heart - drug effects Male Medical sciences Methacholine Chloride Methacholine Compounds - pharmacology Parasympathomimetics - pharmacology Rats Ventricular Fibrillation - etiology Ventricular Fibrillation - physiopathology |
title | The influence of cardiac cholinergic activation on the induction and maintenance of ventricular fibrillation |
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