Stress triggers different pathophysiological mechanisms in younger and older cardiomyopathic hamsters
Because cardiomyopathic hamsters (CMHs) in the lesion-forming period of their disease are more susceptible to the lethal effects of stress than older CMHs, we tested the hypothesis that different pathophysiological effects of stress may occur: coronary vasospasm in younger CMHs and congestive heart...
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Veröffentlicht in: | Cardiovascular research 1995-12, Vol.30 (6), p.985-991 |
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description | Because cardiomyopathic hamsters (CMHs) in the lesion-forming period of their disease are more susceptible to the lethal effects of stress than older CMHs, we tested the hypothesis that different pathophysiological effects of stress may occur: coronary vasospasm in younger CMHs and congestive heart failure in older ones.
CMHs aged 2.5 and 6.5 months were stressed with 2 h supine cold immobilization for 5 consecutive days. Three, 5 and 7 days after stress, the hearts were excised and perfused using a modified Langendorff system. Maximum +/- dP/dt, developed pressure, ventricular relaxation time (Tau) and coronary vascular resistance (CVR) were recorded and CVR was also measured following coronary infusion of arginine vasopressin (AVP).
Stress produced ventricular dysfunction (decreased maximum +/- dP/dt, developed pressure, and increased Tau) in older CMHs (P < 0.05) but not in younger CMHs. Baseline CVR in younger CMHs was significantly higher than in older CMHs (P < 0.01) and AVP infusion produced a bigger increase in CVR in younger stressed CMHs than in either younger nonstressed or older stressed CMHs (P < 0.05).
The younger CMH heart exhibits greater resting vascular tone and stress produces coronary vasoconstriction that is consistent with coronary spasm. In contrast, the older CMH experiences a decrease in cardiac function which remains 7 days after stress and indicates an exacerbation of CHF from the mild form existing prior to stress. The lethal effects of stress may occur because of the activation of different pathological processes in younger and older CMHs. |
doi_str_mv | 10.1016/0008-6363(95)00165-4 |
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CMHs aged 2.5 and 6.5 months were stressed with 2 h supine cold immobilization for 5 consecutive days. Three, 5 and 7 days after stress, the hearts were excised and perfused using a modified Langendorff system. Maximum +/- dP/dt, developed pressure, ventricular relaxation time (Tau) and coronary vascular resistance (CVR) were recorded and CVR was also measured following coronary infusion of arginine vasopressin (AVP).
Stress produced ventricular dysfunction (decreased maximum +/- dP/dt, developed pressure, and increased Tau) in older CMHs (P < 0.05) but not in younger CMHs. Baseline CVR in younger CMHs was significantly higher than in older CMHs (P < 0.01) and AVP infusion produced a bigger increase in CVR in younger stressed CMHs than in either younger nonstressed or older stressed CMHs (P < 0.05).
The younger CMH heart exhibits greater resting vascular tone and stress produces coronary vasoconstriction that is consistent with coronary spasm. In contrast, the older CMH experiences a decrease in cardiac function which remains 7 days after stress and indicates an exacerbation of CHF from the mild form existing prior to stress. The lethal effects of stress may occur because of the activation of different pathological processes in younger and older CMHs.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1016/0008-6363(95)00165-4</identifier><identifier>PMID: 8746215</identifier><identifier>CODEN: CVREAU</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Age Factors ; Aging - physiology ; Animals ; Arginine Vasopressin - pharmacology ; Biological and medical sciences ; Cardiology. Vascular system ; Cardiomyopathies - physiopathology ; Coronary Vasospasm - physiopathology ; Coronary Vessels ; Cricetinae ; Heart ; Heart - physiopathology ; Heart Failure - physiopathology ; Medical sciences ; Myocarditis. Cardiomyopathies ; Stress, Psychological ; Vascular Resistance - drug effects ; Vascular Resistance - physiology</subject><ispartof>Cardiovascular research, 1995-12, Vol.30 (6), p.985-991</ispartof><rights>1996 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=2950516$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8746215$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>QIANG CHANG</creatorcontrib><creatorcontrib>NATELSON, B. H</creatorcontrib><creatorcontrib>OTTENWELLER, J. E</creatorcontrib><creatorcontrib>CONWAY, R. S</creatorcontrib><title>Stress triggers different pathophysiological mechanisms in younger and older cardiomyopathic hamsters</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>Because cardiomyopathic hamsters (CMHs) in the lesion-forming period of their disease are more susceptible to the lethal effects of stress than older CMHs, we tested the hypothesis that different pathophysiological effects of stress may occur: coronary vasospasm in younger CMHs and congestive heart failure in older ones.
CMHs aged 2.5 and 6.5 months were stressed with 2 h supine cold immobilization for 5 consecutive days. Three, 5 and 7 days after stress, the hearts were excised and perfused using a modified Langendorff system. Maximum +/- dP/dt, developed pressure, ventricular relaxation time (Tau) and coronary vascular resistance (CVR) were recorded and CVR was also measured following coronary infusion of arginine vasopressin (AVP).
Stress produced ventricular dysfunction (decreased maximum +/- dP/dt, developed pressure, and increased Tau) in older CMHs (P < 0.05) but not in younger CMHs. Baseline CVR in younger CMHs was significantly higher than in older CMHs (P < 0.01) and AVP infusion produced a bigger increase in CVR in younger stressed CMHs than in either younger nonstressed or older stressed CMHs (P < 0.05).
The younger CMH heart exhibits greater resting vascular tone and stress produces coronary vasoconstriction that is consistent with coronary spasm. In contrast, the older CMH experiences a decrease in cardiac function which remains 7 days after stress and indicates an exacerbation of CHF from the mild form existing prior to stress. The lethal effects of stress may occur because of the activation of different pathological processes in younger and older CMHs.</description><subject>Age Factors</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Arginine Vasopressin - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cardiomyopathies - physiopathology</subject><subject>Coronary Vasospasm - physiopathology</subject><subject>Coronary Vessels</subject><subject>Cricetinae</subject><subject>Heart</subject><subject>Heart - physiopathology</subject><subject>Heart Failure - physiopathology</subject><subject>Medical sciences</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Stress, Psychological</subject><subject>Vascular Resistance - drug effects</subject><subject>Vascular Resistance - physiology</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kEtLAzEUhYMotT7-gUIWIroYTWbyXErxBYILdR3STNJGZiY1d7rovzfVUrhwX-ecxYfQBSV3lFBxTwhRlWhEc6P5LSkXXrEDNKWS86qpGT9E073kGJ0AfJeVc8kmaKIkEzXlU-Q_xuwB8JjjYuEz4DaG4LMfRryy4zKtlhuIqUuL6GyHe--WdojQA44D3qT1UDzYDi1OXVsmZ3MbU79JW290eGl7GEvqGToKtgN_vuun6Ovp8XP2Ur29P7_OHt4qV9N6rHTggloaGJ-3Us-p0pJKJ0uFWihG2Vx7SjSjQUhu20Y3jVOEKeG1Jkrx5hRd_-eucvpZexhNH8H5rrODT2swUiqla0mKkP0LXU4A2QezyrG3eWMoMVu6ZovObNEZzc0fXcOK7XKXv573vt2bdjjL_2r3t1B4hWwHF2EvqzUnnIrmF4tKgv0</recordid><startdate>19951201</startdate><enddate>19951201</enddate><creator>QIANG CHANG</creator><creator>NATELSON, B. H</creator><creator>OTTENWELLER, J. E</creator><creator>CONWAY, R. S</creator><general>Oxford University Press</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>19951201</creationdate><title>Stress triggers different pathophysiological mechanisms in younger and older cardiomyopathic hamsters</title><author>QIANG CHANG ; NATELSON, B. H ; OTTENWELLER, J. E ; CONWAY, R. S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c212t-9f561a1f45bd79b189717c77c7f268414b9e10941f675ad3933c80486e9908853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Age Factors</topic><topic>Aging - physiology</topic><topic>Animals</topic><topic>Arginine Vasopressin - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cardiomyopathies - physiopathology</topic><topic>Coronary Vasospasm - physiopathology</topic><topic>Coronary Vessels</topic><topic>Cricetinae</topic><topic>Heart</topic><topic>Heart - physiopathology</topic><topic>Heart Failure - physiopathology</topic><topic>Medical sciences</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Stress, Psychological</topic><topic>Vascular Resistance - drug effects</topic><topic>Vascular Resistance - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>QIANG CHANG</creatorcontrib><creatorcontrib>NATELSON, B. H</creatorcontrib><creatorcontrib>OTTENWELLER, J. E</creatorcontrib><creatorcontrib>CONWAY, R. S</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>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>QIANG CHANG</au><au>NATELSON, B. H</au><au>OTTENWELLER, J. E</au><au>CONWAY, R. S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stress triggers different pathophysiological mechanisms in younger and older cardiomyopathic hamsters</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>1995-12-01</date><risdate>1995</risdate><volume>30</volume><issue>6</issue><spage>985</spage><epage>991</epage><pages>985-991</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><coden>CVREAU</coden><abstract>Because cardiomyopathic hamsters (CMHs) in the lesion-forming period of their disease are more susceptible to the lethal effects of stress than older CMHs, we tested the hypothesis that different pathophysiological effects of stress may occur: coronary vasospasm in younger CMHs and congestive heart failure in older ones.
CMHs aged 2.5 and 6.5 months were stressed with 2 h supine cold immobilization for 5 consecutive days. Three, 5 and 7 days after stress, the hearts were excised and perfused using a modified Langendorff system. Maximum +/- dP/dt, developed pressure, ventricular relaxation time (Tau) and coronary vascular resistance (CVR) were recorded and CVR was also measured following coronary infusion of arginine vasopressin (AVP).
Stress produced ventricular dysfunction (decreased maximum +/- dP/dt, developed pressure, and increased Tau) in older CMHs (P < 0.05) but not in younger CMHs. Baseline CVR in younger CMHs was significantly higher than in older CMHs (P < 0.01) and AVP infusion produced a bigger increase in CVR in younger stressed CMHs than in either younger nonstressed or older stressed CMHs (P < 0.05).
The younger CMH heart exhibits greater resting vascular tone and stress produces coronary vasoconstriction that is consistent with coronary spasm. In contrast, the older CMH experiences a decrease in cardiac function which remains 7 days after stress and indicates an exacerbation of CHF from the mild form existing prior to stress. The lethal effects of stress may occur because of the activation of different pathological processes in younger and older CMHs.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>8746215</pmid><doi>10.1016/0008-6363(95)00165-4</doi><tpages>7</tpages></addata></record> |
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subjects | Age Factors Aging - physiology Animals Arginine Vasopressin - pharmacology Biological and medical sciences Cardiology. Vascular system Cardiomyopathies - physiopathology Coronary Vasospasm - physiopathology Coronary Vessels Cricetinae Heart Heart - physiopathology Heart Failure - physiopathology Medical sciences Myocarditis. Cardiomyopathies Stress, Psychological Vascular Resistance - drug effects Vascular Resistance - physiology |
title | Stress triggers different pathophysiological mechanisms in younger and older cardiomyopathic hamsters |
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