Post-Endsystolic Active Shortening in the Non-Ischemic Region Impairs Left Ventricular Pressure Fall in Acute Ischemic Heart
To investigate the relation between the impairment of isovolumic relaxation and the regional wall motion in acute ischemia, the left ventricular pressure fall and regional myocardial motion were examined in the relaxation phase in dogs during both acute coronary artery occlusion (n=12) and a regiona...
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| Veröffentlicht in: | The Tohoku Journal of Experimental Medicine 2002, Vol.198(2), pp.107-118 |
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| creator | HOZAWA, HIDENARI SAKUMA, MASAHITO NAKAGAWA, MAKOTO ISHIGAKI, HIDEHIKO KOMAKI, KOHTAROH YAMAMOTO, YOSHITO IKEDA, JUN KAGAYA, YUTAKA WATANABE, JUN SHIRATO, KUNIO |
| description | To investigate the relation between the impairment of isovolumic relaxation and the regional wall motion in acute ischemia, the left ventricular pressure fall and regional myocardial motion were examined in the relaxation phase in dogs during both acute coronary artery occlusion (n=12) and a regional coronary flow reduction (n=6). Fifteen to 40 seconds after complete coronary artery occlusion or in the stable state after a regional coronary flow reduction by 70 to 90% of the control state, a shortening of the non-ischemic region at the early isovolumic relaxation phase (the post-endsystolic shortening) appeared, combined with lengthening of the ischemic region. In these situations, the logarithmic plots of the left ventricular pressure fall was composed of two components (time constant of early part [Ta] and at latter part [Tb]). Ta was greater than Tb (64.3±13.8 milliseconds vs. 36.6±10.4 milliseconds at 15 seconds after coronary occlusion, p |
| doi_str_mv | 10.1620/tjem.198.107 |
| format | Article |
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Fifteen to 40 seconds after complete coronary artery occlusion or in the stable state after a regional coronary flow reduction by 70 to 90% of the control state, a shortening of the non-ischemic region at the early isovolumic relaxation phase (the post-endsystolic shortening) appeared, combined with lengthening of the ischemic region. In these situations, the logarithmic plots of the left ventricular pressure fall was composed of two components (time constant of early part [Ta] and at latter part [Tb]). Ta was greater than Tb (64.3±13.8 milliseconds vs. 36.6±10.4 milliseconds at 15 seconds after coronary occlusion, p<0.01; 67.6±22.9 milliseconds vs. 45.1±17.5 milliseconds at flow reduction, p<0.01) and the time constant at control (p<0.01). These findings suggested that post-endsystolic shortening in the non-ischemic region played a role in a the non-uniformity of the left ventricular contraction and contributed to the impairment of the left ventricular pressure fall in acute regional ischemia, especially in early isovolumic relaxation.</description><identifier>ISSN: 0040-8727</identifier><identifier>EISSN: 1349-3329</identifier><identifier>DOI: 10.1620/tjem.198.107</identifier><identifier>PMID: 12512995</identifier><language>eng</language><publisher>Japan: Tohoku University Medical Press</publisher><subject>Acute Disease ; Animals ; Coronary Circulation ; Dogs ; Electrocardiography ; Heart - physiopathology ; Hemodynamics ; ischemic heart ; Myocardial Contraction ; Myocardial Ischemia - complications ; Myocardial Ischemia - physiopathology ; Pressure ; relaxation ; Systole ; time constant ; Ventricular Dysfunction, Left - etiology ; Ventricular Dysfunction, Left - physiopathology</subject><ispartof>The Tohoku Journal of Experimental Medicine, 2002, Vol.198(2), pp.107-118</ispartof><rights>2002 Tohoku University Medical Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c577t-d4bcc598f6ed7a2f6ee33841facbe79d4b71952db26a2d4a43386d86c77adb1e3</citedby><cites>FETCH-LOGICAL-c577t-d4bcc598f6ed7a2f6ee33841facbe79d4b71952db26a2d4a43386d86c77adb1e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12512995$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HOZAWA, HIDENARI</creatorcontrib><creatorcontrib>SAKUMA, MASAHITO</creatorcontrib><creatorcontrib>NAKAGAWA, MAKOTO</creatorcontrib><creatorcontrib>ISHIGAKI, HIDEHIKO</creatorcontrib><creatorcontrib>KOMAKI, KOHTAROH</creatorcontrib><creatorcontrib>YAMAMOTO, YOSHITO</creatorcontrib><creatorcontrib>IKEDA, JUN</creatorcontrib><creatorcontrib>KAGAYA, YUTAKA</creatorcontrib><creatorcontrib>WATANABE, JUN</creatorcontrib><creatorcontrib>SHIRATO, KUNIO</creatorcontrib><title>Post-Endsystolic Active Shortening in the Non-Ischemic Region Impairs Left Ventricular Pressure Fall in Acute Ischemic Heart</title><title>The Tohoku Journal of Experimental Medicine</title><addtitle>Tohoku J. Exp. Med.</addtitle><description>To investigate the relation between the impairment of isovolumic relaxation and the regional wall motion in acute ischemia, the left ventricular pressure fall and regional myocardial motion were examined in the relaxation phase in dogs during both acute coronary artery occlusion (n=12) and a regional coronary flow reduction (n=6). Fifteen to 40 seconds after complete coronary artery occlusion or in the stable state after a regional coronary flow reduction by 70 to 90% of the control state, a shortening of the non-ischemic region at the early isovolumic relaxation phase (the post-endsystolic shortening) appeared, combined with lengthening of the ischemic region. In these situations, the logarithmic plots of the left ventricular pressure fall was composed of two components (time constant of early part [Ta] and at latter part [Tb]). Ta was greater than Tb (64.3±13.8 milliseconds vs. 36.6±10.4 milliseconds at 15 seconds after coronary occlusion, p<0.01; 67.6±22.9 milliseconds vs. 45.1±17.5 milliseconds at flow reduction, p<0.01) and the time constant at control (p<0.01). These findings suggested that post-endsystolic shortening in the non-ischemic region played a role in a the non-uniformity of the left ventricular contraction and contributed to the impairment of the left ventricular pressure fall in acute regional ischemia, especially in early isovolumic relaxation.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Coronary Circulation</subject><subject>Dogs</subject><subject>Electrocardiography</subject><subject>Heart - physiopathology</subject><subject>Hemodynamics</subject><subject>ischemic heart</subject><subject>Myocardial Contraction</subject><subject>Myocardial Ischemia - complications</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Pressure</subject><subject>relaxation</subject><subject>Systole</subject><subject>time constant</subject><subject>Ventricular Dysfunction, Left - etiology</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><issn>0040-8727</issn><issn>1349-3329</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtPwzAQhC0EglK4cUY-cSLFdh6Oj6XiUamCitc1cpxN6ypxiu0gIfHjcdVSLjvSzrcj7SB0QcmIZozc-BW0IyryESX8AA1onIgojpk4RANCEhLlnPETdOrcipA4ITw7RieUpZQJkQ7Qz7xzProzlft2vmu0wmPl9Rfg12VnPRhtFlgb7JeAnzoTTZ1aQhuoF1jozuBpu5baOjyD2uMPMN5q1TfS4rkF53oL-F42zSZhrHoPeH__CNL6M3RUy8bB-U6H6P3-7m3yGM2eH6aT8SxSKec-qpJSqVTkdQYVlywIxHGe0FqqErgINqciZVXJMsmqRCbBzao8U5zLqqQQD9HVNndtu88enC9a7RQ0jTTQ9a7gLKdE5GkAr7egsp1zFupibXUr7XdBSbFpu9i0XYS2w4IH_HKX25ctVP_wrt4A3G6BlfNyAXsg_K5VA_9p7G8SvjfVUtoCTPwLGvOVYw</recordid><startdate>20021001</startdate><enddate>20021001</enddate><creator>HOZAWA, HIDENARI</creator><creator>SAKUMA, MASAHITO</creator><creator>NAKAGAWA, MAKOTO</creator><creator>ISHIGAKI, HIDEHIKO</creator><creator>KOMAKI, KOHTAROH</creator><creator>YAMAMOTO, YOSHITO</creator><creator>IKEDA, JUN</creator><creator>KAGAYA, YUTAKA</creator><creator>WATANABE, JUN</creator><creator>SHIRATO, KUNIO</creator><general>Tohoku University Medical Press</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>7X8</scope></search><sort><creationdate>20021001</creationdate><title>Post-Endsystolic Active Shortening in the Non-Ischemic Region Impairs Left Ventricular Pressure Fall in Acute Ischemic Heart</title><author>HOZAWA, HIDENARI ; SAKUMA, MASAHITO ; NAKAGAWA, MAKOTO ; ISHIGAKI, HIDEHIKO ; KOMAKI, KOHTAROH ; YAMAMOTO, YOSHITO ; IKEDA, JUN ; KAGAYA, YUTAKA ; WATANABE, JUN ; SHIRATO, KUNIO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c577t-d4bcc598f6ed7a2f6ee33841facbe79d4b71952db26a2d4a43386d86c77adb1e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Coronary Circulation</topic><topic>Dogs</topic><topic>Electrocardiography</topic><topic>Heart - physiopathology</topic><topic>Hemodynamics</topic><topic>ischemic heart</topic><topic>Myocardial Contraction</topic><topic>Myocardial Ischemia - complications</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Pressure</topic><topic>relaxation</topic><topic>Systole</topic><topic>time constant</topic><topic>Ventricular Dysfunction, Left - etiology</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HOZAWA, HIDENARI</creatorcontrib><creatorcontrib>SAKUMA, MASAHITO</creatorcontrib><creatorcontrib>NAKAGAWA, MAKOTO</creatorcontrib><creatorcontrib>ISHIGAKI, HIDEHIKO</creatorcontrib><creatorcontrib>KOMAKI, KOHTAROH</creatorcontrib><creatorcontrib>YAMAMOTO, YOSHITO</creatorcontrib><creatorcontrib>IKEDA, JUN</creatorcontrib><creatorcontrib>KAGAYA, YUTAKA</creatorcontrib><creatorcontrib>WATANABE, JUN</creatorcontrib><creatorcontrib>SHIRATO, KUNIO</creatorcontrib><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>The Tohoku Journal of Experimental Medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HOZAWA, HIDENARI</au><au>SAKUMA, MASAHITO</au><au>NAKAGAWA, MAKOTO</au><au>ISHIGAKI, HIDEHIKO</au><au>KOMAKI, KOHTAROH</au><au>YAMAMOTO, YOSHITO</au><au>IKEDA, JUN</au><au>KAGAYA, YUTAKA</au><au>WATANABE, JUN</au><au>SHIRATO, KUNIO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Post-Endsystolic Active Shortening in the Non-Ischemic Region Impairs Left Ventricular Pressure Fall in Acute Ischemic Heart</atitle><jtitle>The Tohoku Journal of Experimental Medicine</jtitle><addtitle>Tohoku J. Exp. Med.</addtitle><date>2002-10-01</date><risdate>2002</risdate><volume>198</volume><issue>2</issue><spage>107</spage><epage>118</epage><pages>107-118</pages><issn>0040-8727</issn><eissn>1349-3329</eissn><abstract>To investigate the relation between the impairment of isovolumic relaxation and the regional wall motion in acute ischemia, the left ventricular pressure fall and regional myocardial motion were examined in the relaxation phase in dogs during both acute coronary artery occlusion (n=12) and a regional coronary flow reduction (n=6). Fifteen to 40 seconds after complete coronary artery occlusion or in the stable state after a regional coronary flow reduction by 70 to 90% of the control state, a shortening of the non-ischemic region at the early isovolumic relaxation phase (the post-endsystolic shortening) appeared, combined with lengthening of the ischemic region. In these situations, the logarithmic plots of the left ventricular pressure fall was composed of two components (time constant of early part [Ta] and at latter part [Tb]). Ta was greater than Tb (64.3±13.8 milliseconds vs. 36.6±10.4 milliseconds at 15 seconds after coronary occlusion, p<0.01; 67.6±22.9 milliseconds vs. 45.1±17.5 milliseconds at flow reduction, p<0.01) and the time constant at control (p<0.01). These findings suggested that post-endsystolic shortening in the non-ischemic region played a role in a the non-uniformity of the left ventricular contraction and contributed to the impairment of the left ventricular pressure fall in acute regional ischemia, especially in early isovolumic relaxation.</abstract><cop>Japan</cop><pub>Tohoku University Medical Press</pub><pmid>12512995</pmid><doi>10.1620/tjem.198.107</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease Animals Coronary Circulation Dogs Electrocardiography Heart - physiopathology Hemodynamics ischemic heart Myocardial Contraction Myocardial Ischemia - complications Myocardial Ischemia - physiopathology Pressure relaxation Systole time constant Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - physiopathology |
| title | Post-Endsystolic Active Shortening in the Non-Ischemic Region Impairs Left Ventricular Pressure Fall in Acute Ischemic Heart |
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