Central β-Adrenergic Mechanisms May Modulate Ischemic Ventricular Fibrillation in Pigs
A central noradrenergic process may permit expression of the stress-related increase in cardiac vulnerability to ventricular fibrillation (VF). Thus, the effect of central β-adrenergic receptor blockade with l-propranolol (0.01 and 0.05 mg/kg) on ischemia-induced VF vulnerability was evaluated in th...
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| Veröffentlicht in: | Circulation research 1990-02, Vol.66 (2), p.259-270 |
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| creator | Parker, Gerald W Michael, Lloyd H Hartley, Craig J Skinner, James E Entman, Mark L |
| description | A central noradrenergic process may permit expression of the stress-related increase in cardiac vulnerability to ventricular fibrillation (VF). Thus, the effect of central β-adrenergic receptor blockade with l-propranolol (0.01 and 0.05 mg/kg) on ischemia-induced VF vulnerability was evaluated in the psychologically stressed pig model and compared with Ringerʼs solution and D-propranolol (0.05 mg/kg). The ischemia of a maximum 15-minute left anterior descending coronary artery occlusion was used since we previously determined that pigs surviving 15 minutes usually do not fibrillate. Time to the onset of VF was analyzed by time-to-event analysis and ranged from 0.75 to 13.8 minutes in vulnerable pigs. Intracerebroventricular administration of L-propranolol (0.05 mg/kg) prolonged the time to VF compared with Ringerʼs solution and d-propranolol (p |
| doi_str_mv | 10.1161/01.res.66.2.259 |
| format | Article |
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Thus, the effect of central β-adrenergic receptor blockade with l-propranolol (0.01 and 0.05 mg/kg) on ischemia-induced VF vulnerability was evaluated in the psychologically stressed pig model and compared with Ringerʼs solution and D-propranolol (0.05 mg/kg). The ischemia of a maximum 15-minute left anterior descending coronary artery occlusion was used since we previously determined that pigs surviving 15 minutes usually do not fibrillate. Time to the onset of VF was analyzed by time-to-event analysis and ranged from 0.75 to 13.8 minutes in vulnerable pigs. Intracerebroventricular administration of L-propranolol (0.05 mg/kg) prolonged the time to VF compared with Ringerʼs solution and d-propranolol (p<0.05). The high dose of l-propranolol also reduced the incidence of VF (7/15 fibrillated) compared with Ringerʼs solution (12/12 fibrillated) and d-propranolol (6/7 fibrillated). The lower dose of l-propranolol was without effect on VF vulnerability (7/9 fibrillated). The plasma concentration resulting from central administration of 0.05 mg/kg l-propranolol was found to be 9.05±3.25 ng/ml, which is significantly below therapeutic antiarrhythmic blood levels. We conclude that the reduced vulnerability to ischemia-induced VF after intracerebroventricular administration of propranolol is due to alteration of a central β-adrenergic receptor-mediated phenomenon as opposed to an effect on the heart directly or to nonspecific membrane stabilization.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.res.66.2.259</identifier><identifier>PMID: 2153467</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Adaptation, Physiological ; Animals ; Biological and medical sciences ; Biomechanical Phenomena ; Brain - physiology ; Coronary Disease - complications ; Coronary Disease - physiopathology ; Fundamental and applied biological sciences. Psychology ; Heart ; Heart Rate ; Hemodynamics - drug effects ; Injections, Intraventricular ; Propranolol - pharmacokinetics ; Propranolol - pharmacology ; Reaction Time ; Receptors, Adrenergic, beta - physiology ; Space life sciences ; Swine ; Ventricular Fibrillation - etiology ; Ventricular Fibrillation - physiopathology ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 1990-02, Vol.66 (2), p.259-270</ispartof><rights>1990 American Heart Association, Inc.</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5101-8ee0c1165ec0238001efcc3f72c3929ca4b1fc9f717e04525d35e74b7f10efc3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19585317$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2153467$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Parker, Gerald W</creatorcontrib><creatorcontrib>Michael, Lloyd H</creatorcontrib><creatorcontrib>Hartley, Craig J</creatorcontrib><creatorcontrib>Skinner, James E</creatorcontrib><creatorcontrib>Entman, Mark L</creatorcontrib><title>Central β-Adrenergic Mechanisms May Modulate Ischemic Ventricular Fibrillation in Pigs</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>A central noradrenergic process may permit expression of the stress-related increase in cardiac vulnerability to ventricular fibrillation (VF). Thus, the effect of central β-adrenergic receptor blockade with l-propranolol (0.01 and 0.05 mg/kg) on ischemia-induced VF vulnerability was evaluated in the psychologically stressed pig model and compared with Ringerʼs solution and D-propranolol (0.05 mg/kg). The ischemia of a maximum 15-minute left anterior descending coronary artery occlusion was used since we previously determined that pigs surviving 15 minutes usually do not fibrillate. Time to the onset of VF was analyzed by time-to-event analysis and ranged from 0.75 to 13.8 minutes in vulnerable pigs. Intracerebroventricular administration of L-propranolol (0.05 mg/kg) prolonged the time to VF compared with Ringerʼs solution and d-propranolol (p<0.05). The high dose of l-propranolol also reduced the incidence of VF (7/15 fibrillated) compared with Ringerʼs solution (12/12 fibrillated) and d-propranolol (6/7 fibrillated). The lower dose of l-propranolol was without effect on VF vulnerability (7/9 fibrillated). The plasma concentration resulting from central administration of 0.05 mg/kg l-propranolol was found to be 9.05±3.25 ng/ml, which is significantly below therapeutic antiarrhythmic blood levels. We conclude that the reduced vulnerability to ischemia-induced VF after intracerebroventricular administration of propranolol is due to alteration of a central β-adrenergic receptor-mediated phenomenon as opposed to an effect on the heart directly or to nonspecific membrane stabilization.</description><subject>Adaptation, Physiological</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biomechanical Phenomena</subject><subject>Brain - physiology</subject><subject>Coronary Disease - complications</subject><subject>Coronary Disease - physiopathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heart</subject><subject>Heart Rate</subject><subject>Hemodynamics - drug effects</subject><subject>Injections, Intraventricular</subject><subject>Propranolol - pharmacokinetics</subject><subject>Propranolol - pharmacology</subject><subject>Reaction Time</subject><subject>Receptors, Adrenergic, beta - physiology</subject><subject>Space life sciences</subject><subject>Swine</subject><subject>Ventricular Fibrillation - etiology</subject><subject>Ventricular Fibrillation - physiopathology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkU1PGzEQhq2qFU2hZ05Ieym3XWb8sY6PKAKKRNSqoPZoOc4scdkPsHeF-Fv9IfwmHCWip9HM-8yr8WvGjhEqxBrPAKtIqarrildcmQ9shorLUiqNH9kMAEyphYDP7EtKfwFQCm4O2AFHJWStZ-zPgvoxurZ4_VeeryP1FO-DL5bkN64PqUvF0r0Uy2E9tW6k4jr5DXUZ-L1dCz5PY3EZVjG0WQ9DX4S--Bnu0xH71Lg20dd9PWR3lxd3i-_lzY-r68X5TekVApZzIvD5IYo8cDHPB1LjvWg098Jw451cYeNNo1ETSMXVWijScqUbhEyKQ3a6s32Mw9NEabRdSJ7yMT0NU7LaKIO6lhk824E-DilFauxjDJ2LLxbBbpO0gPbXxa2ta8ttTjJvnOytp1VH63d-H13Wv-11l7xrm-h6H9J_W6PmSuCWkzvueWhHiumhnZ4p2g25dtzY_EMgAHmJxgDw3JXbEYo3d9WMHQ</recordid><startdate>199002</startdate><enddate>199002</enddate><creator>Parker, Gerald W</creator><creator>Michael, Lloyd H</creator><creator>Hartley, Craig J</creator><creator>Skinner, James E</creator><creator>Entman, Mark L</creator><general>American Heart Association, Inc</general><general>Lippincott</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>199002</creationdate><title>Central β-Adrenergic Mechanisms May Modulate Ischemic Ventricular Fibrillation in Pigs</title><author>Parker, Gerald W ; Michael, Lloyd H ; Hartley, Craig J ; Skinner, James E ; Entman, Mark L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5101-8ee0c1165ec0238001efcc3f72c3929ca4b1fc9f717e04525d35e74b7f10efc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Adaptation, Physiological</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biomechanical Phenomena</topic><topic>Brain - physiology</topic><topic>Coronary Disease - complications</topic><topic>Coronary Disease - physiopathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heart</topic><topic>Heart Rate</topic><topic>Hemodynamics - drug effects</topic><topic>Injections, Intraventricular</topic><topic>Propranolol - pharmacokinetics</topic><topic>Propranolol - pharmacology</topic><topic>Reaction Time</topic><topic>Receptors, Adrenergic, beta - physiology</topic><topic>Space life sciences</topic><topic>Swine</topic><topic>Ventricular Fibrillation - etiology</topic><topic>Ventricular Fibrillation - physiopathology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Parker, Gerald W</creatorcontrib><creatorcontrib>Michael, Lloyd H</creatorcontrib><creatorcontrib>Hartley, Craig J</creatorcontrib><creatorcontrib>Skinner, James E</creatorcontrib><creatorcontrib>Entman, Mark L</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 research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Parker, Gerald W</au><au>Michael, Lloyd H</au><au>Hartley, Craig J</au><au>Skinner, James E</au><au>Entman, Mark L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Central β-Adrenergic Mechanisms May Modulate Ischemic Ventricular Fibrillation in Pigs</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1990-02</date><risdate>1990</risdate><volume>66</volume><issue>2</issue><spage>259</spage><epage>270</epage><pages>259-270</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>A central noradrenergic process may permit expression of the stress-related increase in cardiac vulnerability to ventricular fibrillation (VF). Thus, the effect of central β-adrenergic receptor blockade with l-propranolol (0.01 and 0.05 mg/kg) on ischemia-induced VF vulnerability was evaluated in the psychologically stressed pig model and compared with Ringerʼs solution and D-propranolol (0.05 mg/kg). The ischemia of a maximum 15-minute left anterior descending coronary artery occlusion was used since we previously determined that pigs surviving 15 minutes usually do not fibrillate. Time to the onset of VF was analyzed by time-to-event analysis and ranged from 0.75 to 13.8 minutes in vulnerable pigs. Intracerebroventricular administration of L-propranolol (0.05 mg/kg) prolonged the time to VF compared with Ringerʼs solution and d-propranolol (p<0.05). The high dose of l-propranolol also reduced the incidence of VF (7/15 fibrillated) compared with Ringerʼs solution (12/12 fibrillated) and d-propranolol (6/7 fibrillated). The lower dose of l-propranolol was without effect on VF vulnerability (7/9 fibrillated). The plasma concentration resulting from central administration of 0.05 mg/kg l-propranolol was found to be 9.05±3.25 ng/ml, which is significantly below therapeutic antiarrhythmic blood levels. We conclude that the reduced vulnerability to ischemia-induced VF after intracerebroventricular administration of propranolol is due to alteration of a central β-adrenergic receptor-mediated phenomenon as opposed to an effect on the heart directly or to nonspecific membrane stabilization.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>2153467</pmid><doi>10.1161/01.res.66.2.259</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Adaptation, Physiological Animals Biological and medical sciences Biomechanical Phenomena Brain - physiology Coronary Disease - complications Coronary Disease - physiopathology Fundamental and applied biological sciences. Psychology Heart Heart Rate Hemodynamics - drug effects Injections, Intraventricular Propranolol - pharmacokinetics Propranolol - pharmacology Reaction Time Receptors, Adrenergic, beta - physiology Space life sciences Swine Ventricular Fibrillation - etiology Ventricular Fibrillation - physiopathology Vertebrates: cardiovascular system |
| title | Central β-Adrenergic Mechanisms May Modulate Ischemic Ventricular Fibrillation in Pigs |
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