Hyperdynamic circulation of arteriovenous fistula preconditions the heart and limits infarct size
Background. Chronic arteriovenous fistulae (AVF) create sustained hyperdynamic circulation. It is not known whether hyperdynamic circulation alters myocardial sensitivity to ischemia and reperfusion injury. We tested the hypothesis that AVF activate molecular responses that increase tolerance to inf...
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| Veröffentlicht in: | The Annals of thoracic surgery 1999-07, Vol.68 (1), p.22-28 |
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| container_title | The Annals of thoracic surgery |
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| creator | Mahgoub, Mahmoud A Guo, Jian-Hau Gao, Shi-Ping Taher, Mohiuddin M Salter, David D Wechsler, Andrew S Abd-Elfattah, Anwar S |
| description | Background. Chronic arteriovenous fistulae (AVF) create sustained hyperdynamic circulation. It is not known whether hyperdynamic circulation alters myocardial sensitivity to ischemia and reperfusion injury. We tested the hypothesis that AVF activate molecular responses that increase tolerance to infarction in dogs.
Methods. Twelve dogs were divided into two groups: 1) AVF group, where an AVF in the femoral region was done; and 2) sham-operated group (each n = 6). After 8 weeks, left ventricular performance was determined from stroke work/end-diastolic length relationship. Myocardial biopsy was obtained to determine heat-shock protein 70 and adenosine triphosphate (ATP) pool. Left anterior descending coronary artery was occluded for 90 minutes at 37°C, followed by 4 hours of reperfusion. Coronary blood flow was determined using different colored microspheres.
Results. The fistula group showed improvement of left ventricular performance (p = 0.03). The infarct size was significantly lower in the fistula group; it was 9.2 ± 2.0% in the fistula group versus 28.4 ± 5.2% in the sham group (p < 0.05). ATP depletion during ischemia was less in the fistula group (p = 0.02). Regional myocardial blood flow was significantly higher in the fistula group (p = 0.03).
Conclusions. Peripheral AVF improve the left ventricular performance, and decrease infarct size and ATP depletion. This protective effect is caused by the development of collaterals in the coronary circulation without expression of heat-shock protein 70. |
| doi_str_mv | 10.1016/S0003-4975(99)00277-5 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69920849</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0003497599002775</els_id><sourcerecordid>69920849</sourcerecordid><originalsourceid>FETCH-LOGICAL-c424t-2adcdae1dfa69931ba86d2dd1077fa60925c04ea11af5259f8cf9a9c21901543</originalsourceid><addsrcrecordid>eNqFkM9LHDEUgENpqVvtn9CSQ5H2MJpkJjObk4i0VRB60Ht4Ji_4ykxmTbLC-tebdZfWm6fw8r7362PsixQnUsj-9EYI0TadGfR3Y34IoYah0e_YQmqtml5p854t_iEH7FPOf2uoavojO5CiU1IKs2BwuVlh8psIEznuKLn1CIXmyOfAIRVMND9inNeZB8qlJvkqoZujpy2VeblHfo-V5BA9H2mikjnFAMkVnukJj9iHAGPGz_v3kN3--nl7cdlc__l9dXF-3bhOdaVR4J0HlD5Ab0wr72DZe-W9FMNQv4RR2okOQUoIup4Xli4YME5JI6Tu2kN2vGu7SvPDGnOxE2WH4wgR6_a2NlVi2ZkK6h3o0pxzwmBXiSZIGyuF3aq1L2rt1ps1xr6otbrWfd0PWN9N6F9V7VxW4NsegOxgDAmio_yfW5q-VW3FznYYVhmPhMlmRxgdeqpii_UzvbHJMzckl6U</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>69920849</pqid></control><display><type>article</type><title>Hyperdynamic circulation of arteriovenous fistula preconditions the heart and limits infarct size</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Mahgoub, Mahmoud A ; Guo, Jian-Hau ; Gao, Shi-Ping ; Taher, Mohiuddin M ; Salter, David D ; Wechsler, Andrew S ; Abd-Elfattah, Anwar S</creator><creatorcontrib>Mahgoub, Mahmoud A ; Guo, Jian-Hau ; Gao, Shi-Ping ; Taher, Mohiuddin M ; Salter, David D ; Wechsler, Andrew S ; Abd-Elfattah, Anwar S</creatorcontrib><description>Background. Chronic arteriovenous fistulae (AVF) create sustained hyperdynamic circulation. It is not known whether hyperdynamic circulation alters myocardial sensitivity to ischemia and reperfusion injury. We tested the hypothesis that AVF activate molecular responses that increase tolerance to infarction in dogs.
Methods. Twelve dogs were divided into two groups: 1) AVF group, where an AVF in the femoral region was done; and 2) sham-operated group (each n = 6). After 8 weeks, left ventricular performance was determined from stroke work/end-diastolic length relationship. Myocardial biopsy was obtained to determine heat-shock protein 70 and adenosine triphosphate (ATP) pool. Left anterior descending coronary artery was occluded for 90 minutes at 37°C, followed by 4 hours of reperfusion. Coronary blood flow was determined using different colored microspheres.
Results. The fistula group showed improvement of left ventricular performance (p = 0.03). The infarct size was significantly lower in the fistula group; it was 9.2 ± 2.0% in the fistula group versus 28.4 ± 5.2% in the sham group (p < 0.05). ATP depletion during ischemia was less in the fistula group (p = 0.02). Regional myocardial blood flow was significantly higher in the fistula group (p = 0.03).
Conclusions. Peripheral AVF improve the left ventricular performance, and decrease infarct size and ATP depletion. This protective effect is caused by the development of collaterals in the coronary circulation without expression of heat-shock protein 70.</description><identifier>ISSN: 0003-4975</identifier><identifier>EISSN: 1552-6259</identifier><identifier>DOI: 10.1016/S0003-4975(99)00277-5</identifier><identifier>PMID: 10421109</identifier><identifier>CODEN: ATHSAK</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adenosine Triphosphate - metabolism ; Animals ; Arteriovenous Fistula - physiopathology ; Arteriovenous Shunt, Surgical ; Biological and medical sciences ; Cardiac Output ; Collateral Circulation ; Coronary Circulation ; Dogs ; Femoral Artery - surgery ; Femoral Vein - surgery ; Hemodynamics ; HSP70 Heat-Shock Proteins - metabolism ; Ischemic Preconditioning, Myocardial ; Medical sciences ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Myocardium - metabolism ; Myocardium - pathology ; Stroke Volume ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the heart ; Ventricular Function, Left</subject><ispartof>The Annals of thoracic surgery, 1999-07, Vol.68 (1), p.22-28</ispartof><rights>1999 The Society of Thoracic Surgeons</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c424t-2adcdae1dfa69931ba86d2dd1077fa60925c04ea11af5259f8cf9a9c21901543</citedby><cites>FETCH-LOGICAL-c424t-2adcdae1dfa69931ba86d2dd1077fa60925c04ea11af5259f8cf9a9c21901543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0003497599002775$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1896323$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10421109$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mahgoub, Mahmoud A</creatorcontrib><creatorcontrib>Guo, Jian-Hau</creatorcontrib><creatorcontrib>Gao, Shi-Ping</creatorcontrib><creatorcontrib>Taher, Mohiuddin M</creatorcontrib><creatorcontrib>Salter, David D</creatorcontrib><creatorcontrib>Wechsler, Andrew S</creatorcontrib><creatorcontrib>Abd-Elfattah, Anwar S</creatorcontrib><title>Hyperdynamic circulation of arteriovenous fistula preconditions the heart and limits infarct size</title><title>The Annals of thoracic surgery</title><addtitle>Ann Thorac Surg</addtitle><description>Background. Chronic arteriovenous fistulae (AVF) create sustained hyperdynamic circulation. It is not known whether hyperdynamic circulation alters myocardial sensitivity to ischemia and reperfusion injury. We tested the hypothesis that AVF activate molecular responses that increase tolerance to infarction in dogs.
Methods. Twelve dogs were divided into two groups: 1) AVF group, where an AVF in the femoral region was done; and 2) sham-operated group (each n = 6). After 8 weeks, left ventricular performance was determined from stroke work/end-diastolic length relationship. Myocardial biopsy was obtained to determine heat-shock protein 70 and adenosine triphosphate (ATP) pool. Left anterior descending coronary artery was occluded for 90 minutes at 37°C, followed by 4 hours of reperfusion. Coronary blood flow was determined using different colored microspheres.
Results. The fistula group showed improvement of left ventricular performance (p = 0.03). The infarct size was significantly lower in the fistula group; it was 9.2 ± 2.0% in the fistula group versus 28.4 ± 5.2% in the sham group (p < 0.05). ATP depletion during ischemia was less in the fistula group (p = 0.02). Regional myocardial blood flow was significantly higher in the fistula group (p = 0.03).
Conclusions. Peripheral AVF improve the left ventricular performance, and decrease infarct size and ATP depletion. This protective effect is caused by the development of collaterals in the coronary circulation without expression of heat-shock protein 70.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Arteriovenous Fistula - physiopathology</subject><subject>Arteriovenous Shunt, Surgical</subject><subject>Biological and medical sciences</subject><subject>Cardiac Output</subject><subject>Collateral Circulation</subject><subject>Coronary Circulation</subject><subject>Dogs</subject><subject>Femoral Artery - surgery</subject><subject>Femoral Vein - surgery</subject><subject>Hemodynamics</subject><subject>HSP70 Heat-Shock Proteins - metabolism</subject><subject>Ischemic Preconditioning, Myocardial</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Stroke Volume</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the heart</subject><subject>Ventricular Function, Left</subject><issn>0003-4975</issn><issn>1552-6259</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM9LHDEUgENpqVvtn9CSQ5H2MJpkJjObk4i0VRB60Ht4Ji_4ykxmTbLC-tebdZfWm6fw8r7362PsixQnUsj-9EYI0TadGfR3Y34IoYah0e_YQmqtml5p854t_iEH7FPOf2uoavojO5CiU1IKs2BwuVlh8psIEznuKLn1CIXmyOfAIRVMND9inNeZB8qlJvkqoZujpy2VeblHfo-V5BA9H2mikjnFAMkVnukJj9iHAGPGz_v3kN3--nl7cdlc__l9dXF-3bhOdaVR4J0HlD5Ab0wr72DZe-W9FMNQv4RR2okOQUoIup4Xli4YME5JI6Tu2kN2vGu7SvPDGnOxE2WH4wgR6_a2NlVi2ZkK6h3o0pxzwmBXiSZIGyuF3aq1L2rt1ps1xr6otbrWfd0PWN9N6F9V7VxW4NsegOxgDAmio_yfW5q-VW3FznYYVhmPhMlmRxgdeqpii_UzvbHJMzckl6U</recordid><startdate>19990701</startdate><enddate>19990701</enddate><creator>Mahgoub, Mahmoud A</creator><creator>Guo, Jian-Hau</creator><creator>Gao, Shi-Ping</creator><creator>Taher, Mohiuddin M</creator><creator>Salter, David D</creator><creator>Wechsler, Andrew S</creator><creator>Abd-Elfattah, Anwar S</creator><general>Elsevier Inc</general><general>Elsevier Science</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>19990701</creationdate><title>Hyperdynamic circulation of arteriovenous fistula preconditions the heart and limits infarct size</title><author>Mahgoub, Mahmoud A ; Guo, Jian-Hau ; Gao, Shi-Ping ; Taher, Mohiuddin M ; Salter, David D ; Wechsler, Andrew S ; Abd-Elfattah, Anwar S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c424t-2adcdae1dfa69931ba86d2dd1077fa60925c04ea11af5259f8cf9a9c21901543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Arteriovenous Fistula - physiopathology</topic><topic>Arteriovenous Shunt, Surgical</topic><topic>Biological and medical sciences</topic><topic>Cardiac Output</topic><topic>Collateral Circulation</topic><topic>Coronary Circulation</topic><topic>Dogs</topic><topic>Femoral Artery - surgery</topic><topic>Femoral Vein - surgery</topic><topic>Hemodynamics</topic><topic>HSP70 Heat-Shock Proteins - metabolism</topic><topic>Ischemic Preconditioning, Myocardial</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Stroke Volume</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the heart</topic><topic>Ventricular Function, Left</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mahgoub, Mahmoud A</creatorcontrib><creatorcontrib>Guo, Jian-Hau</creatorcontrib><creatorcontrib>Gao, Shi-Ping</creatorcontrib><creatorcontrib>Taher, Mohiuddin M</creatorcontrib><creatorcontrib>Salter, David D</creatorcontrib><creatorcontrib>Wechsler, Andrew S</creatorcontrib><creatorcontrib>Abd-Elfattah, Anwar 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>The Annals of thoracic surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mahgoub, Mahmoud A</au><au>Guo, Jian-Hau</au><au>Gao, Shi-Ping</au><au>Taher, Mohiuddin M</au><au>Salter, David D</au><au>Wechsler, Andrew S</au><au>Abd-Elfattah, Anwar S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperdynamic circulation of arteriovenous fistula preconditions the heart and limits infarct size</atitle><jtitle>The Annals of thoracic surgery</jtitle><addtitle>Ann Thorac Surg</addtitle><date>1999-07-01</date><risdate>1999</risdate><volume>68</volume><issue>1</issue><spage>22</spage><epage>28</epage><pages>22-28</pages><issn>0003-4975</issn><eissn>1552-6259</eissn><coden>ATHSAK</coden><abstract>Background. Chronic arteriovenous fistulae (AVF) create sustained hyperdynamic circulation. It is not known whether hyperdynamic circulation alters myocardial sensitivity to ischemia and reperfusion injury. We tested the hypothesis that AVF activate molecular responses that increase tolerance to infarction in dogs.
Methods. Twelve dogs were divided into two groups: 1) AVF group, where an AVF in the femoral region was done; and 2) sham-operated group (each n = 6). After 8 weeks, left ventricular performance was determined from stroke work/end-diastolic length relationship. Myocardial biopsy was obtained to determine heat-shock protein 70 and adenosine triphosphate (ATP) pool. Left anterior descending coronary artery was occluded for 90 minutes at 37°C, followed by 4 hours of reperfusion. Coronary blood flow was determined using different colored microspheres.
Results. The fistula group showed improvement of left ventricular performance (p = 0.03). The infarct size was significantly lower in the fistula group; it was 9.2 ± 2.0% in the fistula group versus 28.4 ± 5.2% in the sham group (p < 0.05). ATP depletion during ischemia was less in the fistula group (p = 0.02). Regional myocardial blood flow was significantly higher in the fistula group (p = 0.03).
Conclusions. Peripheral AVF improve the left ventricular performance, and decrease infarct size and ATP depletion. This protective effect is caused by the development of collaterals in the coronary circulation without expression of heat-shock protein 70.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10421109</pmid><doi>10.1016/S0003-4975(99)00277-5</doi><tpages>7</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adenosine Triphosphate - metabolism Animals Arteriovenous Fistula - physiopathology Arteriovenous Shunt, Surgical Biological and medical sciences Cardiac Output Collateral Circulation Coronary Circulation Dogs Femoral Artery - surgery Femoral Vein - surgery Hemodynamics HSP70 Heat-Shock Proteins - metabolism Ischemic Preconditioning, Myocardial Medical sciences Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardial Infarction - physiopathology Myocardium - metabolism Myocardium - pathology Stroke Volume Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the heart Ventricular Function, Left |
| title | Hyperdynamic circulation of arteriovenous fistula preconditions the heart and limits infarct size |
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