PRECONDITIONING IMPROVES MYOCARDIAL FUNCTION AND REFLOW, BUT NOT VASODILATOR REACTIVITY, AFTER ISCHAEMIA AND REPERFUSION IN ANAESTHETIZED DOGS
SUMMARY 1. The present study examines whether three cycles of brief coronary artery occlusion and reperfusion (i.e. ischaemic preconditioning; PC) can prevent vasodilator dysfunction and the impairment of myocardial reflow caused by prolonged ischaemia. Coronary blood flow, left ventricular dP/dt, s...
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| Veröffentlicht in: | Clinical and experimental pharmacology & physiology 1998-07, Vol.25 (7‐8), p.552-558 |
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| creator | Loke, Kit E. Woodman, Owen L. |
| description | SUMMARY
1. The present study examines whether three cycles of brief coronary artery occlusion and reperfusion (i.e. ischaemic preconditioning; PC) can prevent vasodilator dysfunction and the impairment of myocardial reflow caused by prolonged ischaemia. Coronary blood flow, left ventricular dP/dt, systemic arterial blood pressure and heart rate were measured in open‐chest anaesthetized dogs.
2. Sixty minute occlusion of the left circumflex coronary artery (LCx) and 60 min LCx reperfusion (ISC/REP; group 1) significantly reduced resting coronary blood flow (CBF, initial 29±3mL/min; ISC/REP 20±3mL/min, P |
| doi_str_mv | 10.1111/j.1440-1681.1998.tb02250.x |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_80020776</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>80020776</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3122-a008ae45bd17437062fbe454fb24c62bc1271ff71c912b53acea5900d6c644913</originalsourceid><addsrcrecordid>eNqVkUFvmzAcxa1qU5e1_QiTrB12KuxvYzDsMMkDk1giOAKSqrtYQEBKlCwdNFr7JfaZBwrqfb5Y1u-9Z-k9hD4TsMlwvu5twhhYxPOJTYLAt58roNQF--UKzd7QOzQDB1yL-Bw-oI99vwcAFzznGl0HHncY5TP0d5XJUKeRKpROVTrHarnK9EbmePmoQ5FFSiQ4XqfhyLFII5zJONEP9_jHusCpLvBG5DpSiSh0NjAxCDeqeLzHIi5khlUeLoRcKjF5VzKL1_mYpcY4IfNiIQv1U0Y40vP8Fr1vy0Pf3E33DVrHsggXVqLnKhSJVTuEUqsE8MuGudWWcOZw8GhbDU_WVpTVHq1qQjlpW07qgNDKdcq6Kd0AYOvVHmMBcW7Ql0vuU3f6fW76Z3Pc9XVzOJS_mtO5Nz4ABc69QfjtIqy7U993TWueut2x7F4NATOOYfZmbNyMjZtxDDONYV4G86fpl3N1bLZv1qn9gX-_8D-7Q_P6H8kmlCvXpc4_h5COBA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>80020776</pqid></control><display><type>article</type><title>PRECONDITIONING IMPROVES MYOCARDIAL FUNCTION AND REFLOW, BUT NOT VASODILATOR REACTIVITY, AFTER ISCHAEMIA AND REPERFUSION IN ANAESTHETIZED DOGS</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Loke, Kit E. ; Woodman, Owen L.</creator><creatorcontrib>Loke, Kit E. ; Woodman, Owen L.</creatorcontrib><description>SUMMARY
1. The present study examines whether three cycles of brief coronary artery occlusion and reperfusion (i.e. ischaemic preconditioning; PC) can prevent vasodilator dysfunction and the impairment of myocardial reflow caused by prolonged ischaemia. Coronary blood flow, left ventricular dP/dt, systemic arterial blood pressure and heart rate were measured in open‐chest anaesthetized dogs.
2. Sixty minute occlusion of the left circumflex coronary artery (LCx) and 60 min LCx reperfusion (ISC/REP; group 1) significantly reduced resting coronary blood flow (CBF, initial 29±3mL/min; ISC/REP 20±3mL/min, P<0.05 vx initial) and increased coronary vascular resistance (CVR, initial 4.1±0.6 mmHg/min per mL; ISC/REP 5.8±1.0 mmHg/min per mL, P<0.05 vs initial). By contrast CBF and CVR were not affected in dogs subjected to preconditioning before ischaemia (group 2: CBF, initial 24±4mL/min; PC+ISC/REP 23±4mL/min; CVR, initial 4.7±0.6 mmHg/min per mL; PC+ ISC/REP 5.3±1.0 mmHg/min per mL). These data suggest that ischaemic preconditioning prevents the ischaemia‐induced impairment of myocardial reflow.
3. Ischaemia and reperfusion impaired coronary dilator responses to the endothelium‐dependent dilator acetylcholine (ACBF, after ISC/REP: 50±6% of initial) and the endothelium‐independent dilator glyceryl trinitrate (ΔCBF, ISC/REP: 46±6% of initial). Despite the improvement in reperfusion in the preconditioned group, there was no significant improvement in responses to acetylcholine (PC+ISC/REP 52±6% of initial) or glyceryl trinitrate (PC+ISC/REP 59±6% of initial) after ischaemia and reperfusion.
4. The reduction in left ventricular dP/dt after ischaemia and reperfusion was significantly smaller in the preconditioned group indicating a lower level of impairment of cardiac contractility. In addition, we confirmed that preconditioning caused a significant reduction in infarct size and a reduction in the release of lactate dehydrogenase indicating less cardiac injury.
5. These results suggest that although ischaemic preconditioning was able to improve both myocardial reperfusion and contractility, it was not able to preserve vasodilator function. Such a reduction in vasodilator reserve could prevent adequate myocardial perfusion under conditions of elevated oxygen demand.</description><identifier>ISSN: 0305-1870</identifier><identifier>EISSN: 1440-1681</identifier><identifier>DOI: 10.1111/j.1440-1681.1998.tb02250.x</identifier><identifier>PMID: 9673427</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Acetylcholine - pharmacology ; Animals ; Blood Pressure - drug effects ; coronary blood flow ; Coronary Circulation - drug effects ; Coronary Circulation - physiology ; Dogs ; Female ; Heart - drug effects ; Heart - physiology ; In Vitro Techniques ; ischaemia ; Ischemic Preconditioning, Myocardial ; L-Lactate Dehydrogenase - metabolism ; Male ; Myocardial Infarction - pathology ; Myocardial Ischemia - physiopathology ; Myocardial Reperfusion ; Myocardium - enzymology ; Myocardium - metabolism ; Nitroglycerin - pharmacology ; preconditioning ; Time Factors ; vasodilatation ; Vasodilator Agents - pharmacology</subject><ispartof>Clinical and experimental pharmacology & physiology, 1998-07, Vol.25 (7‐8), p.552-558</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3122-a008ae45bd17437062fbe454fb24c62bc1271ff71c912b53acea5900d6c644913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1440-1681.1998.tb02250.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1440-1681.1998.tb02250.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9673427$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Loke, Kit E.</creatorcontrib><creatorcontrib>Woodman, Owen L.</creatorcontrib><title>PRECONDITIONING IMPROVES MYOCARDIAL FUNCTION AND REFLOW, BUT NOT VASODILATOR REACTIVITY, AFTER ISCHAEMIA AND REPERFUSION IN ANAESTHETIZED DOGS</title><title>Clinical and experimental pharmacology & physiology</title><addtitle>Clin Exp Pharmacol Physiol</addtitle><description>SUMMARY
1. The present study examines whether three cycles of brief coronary artery occlusion and reperfusion (i.e. ischaemic preconditioning; PC) can prevent vasodilator dysfunction and the impairment of myocardial reflow caused by prolonged ischaemia. Coronary blood flow, left ventricular dP/dt, systemic arterial blood pressure and heart rate were measured in open‐chest anaesthetized dogs.
2. Sixty minute occlusion of the left circumflex coronary artery (LCx) and 60 min LCx reperfusion (ISC/REP; group 1) significantly reduced resting coronary blood flow (CBF, initial 29±3mL/min; ISC/REP 20±3mL/min, P<0.05 vx initial) and increased coronary vascular resistance (CVR, initial 4.1±0.6 mmHg/min per mL; ISC/REP 5.8±1.0 mmHg/min per mL, P<0.05 vs initial). By contrast CBF and CVR were not affected in dogs subjected to preconditioning before ischaemia (group 2: CBF, initial 24±4mL/min; PC+ISC/REP 23±4mL/min; CVR, initial 4.7±0.6 mmHg/min per mL; PC+ ISC/REP 5.3±1.0 mmHg/min per mL). These data suggest that ischaemic preconditioning prevents the ischaemia‐induced impairment of myocardial reflow.
3. Ischaemia and reperfusion impaired coronary dilator responses to the endothelium‐dependent dilator acetylcholine (ACBF, after ISC/REP: 50±6% of initial) and the endothelium‐independent dilator glyceryl trinitrate (ΔCBF, ISC/REP: 46±6% of initial). Despite the improvement in reperfusion in the preconditioned group, there was no significant improvement in responses to acetylcholine (PC+ISC/REP 52±6% of initial) or glyceryl trinitrate (PC+ISC/REP 59±6% of initial) after ischaemia and reperfusion.
4. The reduction in left ventricular dP/dt after ischaemia and reperfusion was significantly smaller in the preconditioned group indicating a lower level of impairment of cardiac contractility. In addition, we confirmed that preconditioning caused a significant reduction in infarct size and a reduction in the release of lactate dehydrogenase indicating less cardiac injury.
5. These results suggest that although ischaemic preconditioning was able to improve both myocardial reperfusion and contractility, it was not able to preserve vasodilator function. Such a reduction in vasodilator reserve could prevent adequate myocardial perfusion under conditions of elevated oxygen demand.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>coronary blood flow</subject><subject>Coronary Circulation - drug effects</subject><subject>Coronary Circulation - physiology</subject><subject>Dogs</subject><subject>Female</subject><subject>Heart - drug effects</subject><subject>Heart - physiology</subject><subject>In Vitro Techniques</subject><subject>ischaemia</subject><subject>Ischemic Preconditioning, Myocardial</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Male</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Myocardial Reperfusion</subject><subject>Myocardium - enzymology</subject><subject>Myocardium - metabolism</subject><subject>Nitroglycerin - pharmacology</subject><subject>preconditioning</subject><subject>Time Factors</subject><subject>vasodilatation</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0305-1870</issn><issn>1440-1681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkUFvmzAcxa1qU5e1_QiTrB12KuxvYzDsMMkDk1giOAKSqrtYQEBKlCwdNFr7JfaZBwrqfb5Y1u-9Z-k9hD4TsMlwvu5twhhYxPOJTYLAt58roNQF--UKzd7QOzQDB1yL-Bw-oI99vwcAFzznGl0HHncY5TP0d5XJUKeRKpROVTrHarnK9EbmePmoQ5FFSiQ4XqfhyLFII5zJONEP9_jHusCpLvBG5DpSiSh0NjAxCDeqeLzHIi5khlUeLoRcKjF5VzKL1_mYpcY4IfNiIQv1U0Y40vP8Fr1vy0Pf3E33DVrHsggXVqLnKhSJVTuEUqsE8MuGudWWcOZw8GhbDU_WVpTVHq1qQjlpW07qgNDKdcq6Kd0AYOvVHmMBcW7Ql0vuU3f6fW76Z3Pc9XVzOJS_mtO5Nz4ABc69QfjtIqy7U993TWueut2x7F4NATOOYfZmbNyMjZtxDDONYV4G86fpl3N1bLZv1qn9gX-_8D-7Q_P6H8kmlCvXpc4_h5COBA</recordid><startdate>19980701</startdate><enddate>19980701</enddate><creator>Loke, Kit E.</creator><creator>Woodman, Owen L.</creator><general>Blackwell Publishing Ltd</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>19980701</creationdate><title>PRECONDITIONING IMPROVES MYOCARDIAL FUNCTION AND REFLOW, BUT NOT VASODILATOR REACTIVITY, AFTER ISCHAEMIA AND REPERFUSION IN ANAESTHETIZED DOGS</title><author>Loke, Kit E. ; Woodman, Owen L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3122-a008ae45bd17437062fbe454fb24c62bc1271ff71c912b53acea5900d6c644913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>coronary blood flow</topic><topic>Coronary Circulation - drug effects</topic><topic>Coronary Circulation - physiology</topic><topic>Dogs</topic><topic>Female</topic><topic>Heart - drug effects</topic><topic>Heart - physiology</topic><topic>In Vitro Techniques</topic><topic>ischaemia</topic><topic>Ischemic Preconditioning, Myocardial</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Male</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Myocardial Reperfusion</topic><topic>Myocardium - enzymology</topic><topic>Myocardium - metabolism</topic><topic>Nitroglycerin - pharmacology</topic><topic>preconditioning</topic><topic>Time Factors</topic><topic>vasodilatation</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Loke, Kit E.</creatorcontrib><creatorcontrib>Woodman, Owen L.</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>Clinical and experimental pharmacology & physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Loke, Kit E.</au><au>Woodman, Owen L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PRECONDITIONING IMPROVES MYOCARDIAL FUNCTION AND REFLOW, BUT NOT VASODILATOR REACTIVITY, AFTER ISCHAEMIA AND REPERFUSION IN ANAESTHETIZED DOGS</atitle><jtitle>Clinical and experimental pharmacology & physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>1998-07-01</date><risdate>1998</risdate><volume>25</volume><issue>7‐8</issue><spage>552</spage><epage>558</epage><pages>552-558</pages><issn>0305-1870</issn><eissn>1440-1681</eissn><abstract>SUMMARY
1. The present study examines whether three cycles of brief coronary artery occlusion and reperfusion (i.e. ischaemic preconditioning; PC) can prevent vasodilator dysfunction and the impairment of myocardial reflow caused by prolonged ischaemia. Coronary blood flow, left ventricular dP/dt, systemic arterial blood pressure and heart rate were measured in open‐chest anaesthetized dogs.
2. Sixty minute occlusion of the left circumflex coronary artery (LCx) and 60 min LCx reperfusion (ISC/REP; group 1) significantly reduced resting coronary blood flow (CBF, initial 29±3mL/min; ISC/REP 20±3mL/min, P<0.05 vx initial) and increased coronary vascular resistance (CVR, initial 4.1±0.6 mmHg/min per mL; ISC/REP 5.8±1.0 mmHg/min per mL, P<0.05 vs initial). By contrast CBF and CVR were not affected in dogs subjected to preconditioning before ischaemia (group 2: CBF, initial 24±4mL/min; PC+ISC/REP 23±4mL/min; CVR, initial 4.7±0.6 mmHg/min per mL; PC+ ISC/REP 5.3±1.0 mmHg/min per mL). These data suggest that ischaemic preconditioning prevents the ischaemia‐induced impairment of myocardial reflow.
3. Ischaemia and reperfusion impaired coronary dilator responses to the endothelium‐dependent dilator acetylcholine (ACBF, after ISC/REP: 50±6% of initial) and the endothelium‐independent dilator glyceryl trinitrate (ΔCBF, ISC/REP: 46±6% of initial). Despite the improvement in reperfusion in the preconditioned group, there was no significant improvement in responses to acetylcholine (PC+ISC/REP 52±6% of initial) or glyceryl trinitrate (PC+ISC/REP 59±6% of initial) after ischaemia and reperfusion.
4. The reduction in left ventricular dP/dt after ischaemia and reperfusion was significantly smaller in the preconditioned group indicating a lower level of impairment of cardiac contractility. In addition, we confirmed that preconditioning caused a significant reduction in infarct size and a reduction in the release of lactate dehydrogenase indicating less cardiac injury.
5. These results suggest that although ischaemic preconditioning was able to improve both myocardial reperfusion and contractility, it was not able to preserve vasodilator function. Such a reduction in vasodilator reserve could prevent adequate myocardial perfusion under conditions of elevated oxygen demand.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>9673427</pmid><doi>10.1111/j.1440-1681.1998.tb02250.x</doi><tpages>7</tpages></addata></record> |
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| ispartof | Clinical and experimental pharmacology & physiology, 1998-07, Vol.25 (7‐8), p.552-558 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Acetylcholine - pharmacology Animals Blood Pressure - drug effects coronary blood flow Coronary Circulation - drug effects Coronary Circulation - physiology Dogs Female Heart - drug effects Heart - physiology In Vitro Techniques ischaemia Ischemic Preconditioning, Myocardial L-Lactate Dehydrogenase - metabolism Male Myocardial Infarction - pathology Myocardial Ischemia - physiopathology Myocardial Reperfusion Myocardium - enzymology Myocardium - metabolism Nitroglycerin - pharmacology preconditioning Time Factors vasodilatation Vasodilator Agents - pharmacology |
| title | PRECONDITIONING IMPROVES MYOCARDIAL FUNCTION AND REFLOW, BUT NOT VASODILATOR REACTIVITY, AFTER ISCHAEMIA AND REPERFUSION IN ANAESTHETIZED DOGS |
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