Distribution of a neutral cardioplegic vehicle during the development of ischemic myocardial contracture
During prolonged ischemic cardiac arrest successful myocardial protection depends upon uniform delivery of cardioplegic solutions to all regions of the heart. Accordingly, we studied the regional and transmural distribution of a neutral crystalloid (dextran-saline) solution during normothermic (37°C...
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| Veröffentlicht in: | Journal of molecular and cellular cardiology 1987-10, Vol.19 (10), p.977-989 |
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| creator | Zile, Michael R. Neill, William A. Gaasch, William H. Oxendine, John Apstein, Carl S. Weinberg, Ellen Bing, Oscar H.L. |
| description | During prolonged ischemic cardiac arrest successful myocardial protection depends upon uniform delivery of cardioplegic solutions to all regions of the heart. Accordingly, we studied the regional and transmural distribution of a neutral crystalloid (dextran-saline) solution during normothermic (37°C) ischemia in 18 isolated blood-perfused dog hearts (isovolumic left ventricle). In the baseline state, coronary perfusion pressure was 100 mmHg. At the onset of ischemia and every 15 min throughout ischemia, we infused 100 ml of crystalloid solution (37°C) at a perfusion pressure of 100 mmHg and the distribution of crystalloid solution was assessed (radioactive microsphere technique). The hearts were reperfused after 60 min (
n=9) or 90 mins (
n=9) of ischemia. In the baseline pre-arrest state the left ventricle (LV) received 67±1.0% of the total coronary blood flow; the LV subendocardial to subepicardial flow ratio was 1.33±0.18, the LV end diastolic pressure was 7.5±0.4 mmHg, and mean trasmural myocardial adenosine triphosphate (ATP) was 16.4±1.1 μ
m/g DW. At the onset and throughout the first 45 mins of ischemia (
n=9), regional and transmural distribution of the crystalloid solution was similar to that of coronary blood flow during the baseline state; there was no change in LV end diastolic pressure, but there was a moderate fall in ATP content (7.26±1.6 μm/g DW). After 75 mins of ischemia (
n=9), despite the development of ischemic contracture (LV end diastolic pressure exceeded 20 mmHg in all 9 hearts) and marked ATP depletion (2.76±0.5 μ
m/ g DW), there was an increase in crystalloid solution delivery to the LV as a whole and the subendocardium in particular (the LV received 82±2.0% and the subendocardial to subepicardial flow ratio was 1.75±0.1). Even in a subgroup with severe contracture during ischemic arrest (LV end diastolic pressure >60 mmHg,
n=4) there was no reduction in crystalloid solution delivery. Thus, the presence of ischemic contracture does not preclude delivery of crystalloid solution to the LV subendocardium. |
| doi_str_mv | 10.1016/S0022-2828(87)80570-9 |
| format | Article |
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n=9) or 90 mins (
n=9) of ischemia. In the baseline pre-arrest state the left ventricle (LV) received 67±1.0% of the total coronary blood flow; the LV subendocardial to subepicardial flow ratio was 1.33±0.18, the LV end diastolic pressure was 7.5±0.4 mmHg, and mean trasmural myocardial adenosine triphosphate (ATP) was 16.4±1.1 μ
m/g DW. At the onset and throughout the first 45 mins of ischemia (
n=9), regional and transmural distribution of the crystalloid solution was similar to that of coronary blood flow during the baseline state; there was no change in LV end diastolic pressure, but there was a moderate fall in ATP content (7.26±1.6 μm/g DW). After 75 mins of ischemia (
n=9), despite the development of ischemic contracture (LV end diastolic pressure exceeded 20 mmHg in all 9 hearts) and marked ATP depletion (2.76±0.5 μ
m/ g DW), there was an increase in crystalloid solution delivery to the LV as a whole and the subendocardium in particular (the LV received 82±2.0% and the subendocardial to subepicardial flow ratio was 1.75±0.1). Even in a subgroup with severe contracture during ischemic arrest (LV end diastolic pressure >60 mmHg,
n=4) there was no reduction in crystalloid solution delivery. Thus, the presence of ischemic contracture does not preclude delivery of crystalloid solution to the LV subendocardium.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1016/S0022-2828(87)80570-9</identifier><identifier>PMID: 2449532</identifier><identifier>CODEN: JMCDAY</identifier><language>eng</language><publisher>Kent: Elsevier Ltd</publisher><subject>Adenosine Triphosphate - metabolism ; Anesthesia ; Anesthesia depending on type of surgery ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; Blood Pressure ; Cardioplegia ; Coronary blood flow ; Coronary Circulation ; Coronary Disease - physiopathology ; Dextrans ; Dogs ; Energy Metabolism ; Heart - physiology ; Heart - physiopathology ; Heart Arrest - physiopathology ; Heart Ventricles - physiopathology ; In Vitro Techniques ; Ischemic arrest ; Lactates - metabolism ; Medical sciences ; Myocardial Contraction ; Myocardial contracture ; Oxygen Consumption ; Perfusion ; Phosphocreatine - metabolism ; Thoracic and cardiovascular surgery. Cardiopulmonary bypass ; Ventricular Function</subject><ispartof>Journal of molecular and cellular cardiology, 1987-10, Vol.19 (10), p.977-989</ispartof><rights>1987 Academic Press Limited</rights><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-e0ffefaad20f33c241976643d65c46c423faad5ebb26db0c89bbbc36badf23733</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0022-2828(87)80570-9$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7525111$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2449532$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zile, Michael R.</creatorcontrib><creatorcontrib>Neill, William A.</creatorcontrib><creatorcontrib>Gaasch, William H.</creatorcontrib><creatorcontrib>Oxendine, John</creatorcontrib><creatorcontrib>Apstein, Carl S.</creatorcontrib><creatorcontrib>Weinberg, Ellen</creatorcontrib><creatorcontrib>Bing, Oscar H.L.</creatorcontrib><title>Distribution of a neutral cardioplegic vehicle during the development of ischemic myocardial contracture</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>During prolonged ischemic cardiac arrest successful myocardial protection depends upon uniform delivery of cardioplegic solutions to all regions of the heart. Accordingly, we studied the regional and transmural distribution of a neutral crystalloid (dextran-saline) solution during normothermic (37°C) ischemia in 18 isolated blood-perfused dog hearts (isovolumic left ventricle). In the baseline state, coronary perfusion pressure was 100 mmHg. At the onset of ischemia and every 15 min throughout ischemia, we infused 100 ml of crystalloid solution (37°C) at a perfusion pressure of 100 mmHg and the distribution of crystalloid solution was assessed (radioactive microsphere technique). The hearts were reperfused after 60 min (
n=9) or 90 mins (
n=9) of ischemia. In the baseline pre-arrest state the left ventricle (LV) received 67±1.0% of the total coronary blood flow; the LV subendocardial to subepicardial flow ratio was 1.33±0.18, the LV end diastolic pressure was 7.5±0.4 mmHg, and mean trasmural myocardial adenosine triphosphate (ATP) was 16.4±1.1 μ
m/g DW. At the onset and throughout the first 45 mins of ischemia (
n=9), regional and transmural distribution of the crystalloid solution was similar to that of coronary blood flow during the baseline state; there was no change in LV end diastolic pressure, but there was a moderate fall in ATP content (7.26±1.6 μm/g DW). After 75 mins of ischemia (
n=9), despite the development of ischemic contracture (LV end diastolic pressure exceeded 20 mmHg in all 9 hearts) and marked ATP depletion (2.76±0.5 μ
m/ g DW), there was an increase in crystalloid solution delivery to the LV as a whole and the subendocardium in particular (the LV received 82±2.0% and the subendocardial to subepicardial flow ratio was 1.75±0.1). Even in a subgroup with severe contracture during ischemic arrest (LV end diastolic pressure >60 mmHg,
n=4) there was no reduction in crystalloid solution delivery. Thus, the presence of ischemic contracture does not preclude delivery of crystalloid solution to the LV subendocardium.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Anesthesia</subject><subject>Anesthesia depending on type of surgery</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Cardioplegia</subject><subject>Coronary blood flow</subject><subject>Coronary Circulation</subject><subject>Coronary Disease - physiopathology</subject><subject>Dextrans</subject><subject>Dogs</subject><subject>Energy Metabolism</subject><subject>Heart - physiology</subject><subject>Heart - physiopathology</subject><subject>Heart Arrest - physiopathology</subject><subject>Heart Ventricles - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Ischemic arrest</subject><subject>Lactates - metabolism</subject><subject>Medical sciences</subject><subject>Myocardial Contraction</subject><subject>Myocardial contracture</subject><subject>Oxygen Consumption</subject><subject>Perfusion</subject><subject>Phosphocreatine - metabolism</subject><subject>Thoracic and cardiovascular surgery. Cardiopulmonary bypass</subject><subject>Ventricular Function</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1q3DAUhUVpSadpHyHgRSntwo0sWbK0KiH9hUAWaddCP1cZFduaSvJA3j7yzDDbrnThfufo8iF01eHPHe749QPGhLREEPFRDJ8EZgNu5Qu06bBkrWCif4k2Z-Q1epPzX4yx7Cm9QBek7yWjZIO2X0MuKZilhDg30Te6mWEpSY-N1cmFuBvhMdhmD9tgR2jcksL82JRtHWEPY9xNMJc1GLLdwlTR6SkeomtFnGuVLUuCt-iV12OGd6f3Ev35_u337c_27v7Hr9ubu9ZSIUsL2HvwWjuCPaWW9J0cOO-p48z23PaErksGxhDuDLZCGmMs5UY7T-hA6SX6cOzdpfhvgVzUVC-DcdQzxCWrYZCMSy4qyI6gTTHnBF7tUph0elIdVqthdTCsVn1KDOpgWMmauzp9sJgJ3Dl1Ulr37097na0efdKzDfmMDYywrusq9uWIQZWxD5BUtgFmCy4ksEW5GP5zyDMaIprS</recordid><startdate>19871001</startdate><enddate>19871001</enddate><creator>Zile, Michael R.</creator><creator>Neill, William A.</creator><creator>Gaasch, William H.</creator><creator>Oxendine, John</creator><creator>Apstein, Carl S.</creator><creator>Weinberg, Ellen</creator><creator>Bing, Oscar H.L.</creator><general>Elsevier Ltd</general><general>Elsevier</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>19871001</creationdate><title>Distribution of a neutral cardioplegic vehicle during the development of ischemic myocardial contracture</title><author>Zile, Michael R. ; Neill, William A. ; Gaasch, William H. ; Oxendine, John ; Apstein, Carl S. ; Weinberg, Ellen ; Bing, Oscar H.L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-e0ffefaad20f33c241976643d65c46c423faad5ebb26db0c89bbbc36badf23733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1987</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Anesthesia</topic><topic>Anesthesia depending on type of surgery</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Cardioplegia</topic><topic>Coronary blood flow</topic><topic>Coronary Circulation</topic><topic>Coronary Disease - physiopathology</topic><topic>Dextrans</topic><topic>Dogs</topic><topic>Energy Metabolism</topic><topic>Heart - physiology</topic><topic>Heart - physiopathology</topic><topic>Heart Arrest - physiopathology</topic><topic>Heart Ventricles - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Ischemic arrest</topic><topic>Lactates - metabolism</topic><topic>Medical sciences</topic><topic>Myocardial Contraction</topic><topic>Myocardial contracture</topic><topic>Oxygen Consumption</topic><topic>Perfusion</topic><topic>Phosphocreatine - metabolism</topic><topic>Thoracic and cardiovascular surgery. Cardiopulmonary bypass</topic><topic>Ventricular Function</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zile, Michael R.</creatorcontrib><creatorcontrib>Neill, William A.</creatorcontrib><creatorcontrib>Gaasch, William H.</creatorcontrib><creatorcontrib>Oxendine, John</creatorcontrib><creatorcontrib>Apstein, Carl S.</creatorcontrib><creatorcontrib>Weinberg, Ellen</creatorcontrib><creatorcontrib>Bing, Oscar H.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>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zile, Michael R.</au><au>Neill, William A.</au><au>Gaasch, William H.</au><au>Oxendine, John</au><au>Apstein, Carl S.</au><au>Weinberg, Ellen</au><au>Bing, Oscar H.L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Distribution of a neutral cardioplegic vehicle during the development of ischemic myocardial contracture</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>1987-10-01</date><risdate>1987</risdate><volume>19</volume><issue>10</issue><spage>977</spage><epage>989</epage><pages>977-989</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><coden>JMCDAY</coden><abstract>During prolonged ischemic cardiac arrest successful myocardial protection depends upon uniform delivery of cardioplegic solutions to all regions of the heart. Accordingly, we studied the regional and transmural distribution of a neutral crystalloid (dextran-saline) solution during normothermic (37°C) ischemia in 18 isolated blood-perfused dog hearts (isovolumic left ventricle). In the baseline state, coronary perfusion pressure was 100 mmHg. At the onset of ischemia and every 15 min throughout ischemia, we infused 100 ml of crystalloid solution (37°C) at a perfusion pressure of 100 mmHg and the distribution of crystalloid solution was assessed (radioactive microsphere technique). The hearts were reperfused after 60 min (
n=9) or 90 mins (
n=9) of ischemia. In the baseline pre-arrest state the left ventricle (LV) received 67±1.0% of the total coronary blood flow; the LV subendocardial to subepicardial flow ratio was 1.33±0.18, the LV end diastolic pressure was 7.5±0.4 mmHg, and mean trasmural myocardial adenosine triphosphate (ATP) was 16.4±1.1 μ
m/g DW. At the onset and throughout the first 45 mins of ischemia (
n=9), regional and transmural distribution of the crystalloid solution was similar to that of coronary blood flow during the baseline state; there was no change in LV end diastolic pressure, but there was a moderate fall in ATP content (7.26±1.6 μm/g DW). After 75 mins of ischemia (
n=9), despite the development of ischemic contracture (LV end diastolic pressure exceeded 20 mmHg in all 9 hearts) and marked ATP depletion (2.76±0.5 μ
m/ g DW), there was an increase in crystalloid solution delivery to the LV as a whole and the subendocardium in particular (the LV received 82±2.0% and the subendocardial to subepicardial flow ratio was 1.75±0.1). Even in a subgroup with severe contracture during ischemic arrest (LV end diastolic pressure >60 mmHg,
n=4) there was no reduction in crystalloid solution delivery. Thus, the presence of ischemic contracture does not preclude delivery of crystalloid solution to the LV subendocardium.</abstract><cop>Kent</cop><pub>Elsevier Ltd</pub><pmid>2449532</pmid><doi>10.1016/S0022-2828(87)80570-9</doi><tpages>13</tpages></addata></record> |
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| ispartof | Journal of molecular and cellular cardiology, 1987-10, Vol.19 (10), p.977-989 |
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| subjects | Adenosine Triphosphate - metabolism Anesthesia Anesthesia depending on type of surgery Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Blood Pressure Cardioplegia Coronary blood flow Coronary Circulation Coronary Disease - physiopathology Dextrans Dogs Energy Metabolism Heart - physiology Heart - physiopathology Heart Arrest - physiopathology Heart Ventricles - physiopathology In Vitro Techniques Ischemic arrest Lactates - metabolism Medical sciences Myocardial Contraction Myocardial contracture Oxygen Consumption Perfusion Phosphocreatine - metabolism Thoracic and cardiovascular surgery. Cardiopulmonary bypass Ventricular Function |
| title | Distribution of a neutral cardioplegic vehicle during the development of ischemic myocardial contracture |
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