Adenosine-supplemented blood cardioplegia attenuates postischemic dysfunction after severe regional ischemia
Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO's potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1999-11, Vol.100 (19), p.II376-II383 |
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| creator | THOURANI, V. H RONSON, R. S VAN WYLEN, D. G. L SHEARER, S. T KATZMARK, S. L ZHAO, Z.-Q HAN, D. C GUYTON, R. A VINTEN-JOHANSEN, J |
| description | Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO's potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusion reduces postischemic dysfunction after severe regional ischemia.
After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4 degrees C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27 degrees C BCP was delivered for the terminal infusion. Dogs (n=6 per group) received unsupplemented BCP, ADO (100 micromol/L/L) supplemented in all infusions of BCP (ADO-CP), or ADO (100 micromol x L(-1) x L(-1)) supplemented only in the terminal infusion of BCP followed by intravenous ADO (140 microg x kg(-1) x min(-1)) infusion for the first 30 minutes of reperfusion (ADO-R). Postischemic regional systolic shortening was significantly greater in the ADO-R group (5+/-2.0%) than in the BCP group (-3+/-1.0%), but not in the ADO-CP group (2+/-0.2%). Postischemic regional diastolic stiffness in the area at risk during end reperfusion was lower with ADO-R (1.8+/-0.3%) than with ADO-CP (2.7+/-0.3%) or BCP (4.4+/-0.5%). Infarct size was reduced in the ADO-CP (29+/-2%) and ADO-R (21+/-2%) groups compared with the BCP group (42+/-4%). Edema in the myocardial area at risk was decreased in the ADO-CP (82+/-0.2%) and ADO-R (80+/-0.4%) groups compared with the BCP group (86+/-0.7%). Adherence of fluorescently labeled neutrophils (PMNs) to postischemic coronary artery endothelium was attenuated by ADO-R (55+/-2 PMNs/mm(2)), but not by ADO-CP (114+/-5 PMNs/mm(2)), compared with BCP (118+/-3 PMNs/mm(2)).
The results show that BCP supplemented with ADO reduces infarct size, preserves postischemic systolic and diastolic regional function but does not attenuate coronary artery endothelial dysfunction unless administered during reperfusion. |
| format | Article |
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After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4 degrees C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27 degrees C BCP was delivered for the terminal infusion. Dogs (n=6 per group) received unsupplemented BCP, ADO (100 micromol/L/L) supplemented in all infusions of BCP (ADO-CP), or ADO (100 micromol x L(-1) x L(-1)) supplemented only in the terminal infusion of BCP followed by intravenous ADO (140 microg x kg(-1) x min(-1)) infusion for the first 30 minutes of reperfusion (ADO-R). Postischemic regional systolic shortening was significantly greater in the ADO-R group (5+/-2.0%) than in the BCP group (-3+/-1.0%), but not in the ADO-CP group (2+/-0.2%). Postischemic regional diastolic stiffness in the area at risk during end reperfusion was lower with ADO-R (1.8+/-0.3%) than with ADO-CP (2.7+/-0.3%) or BCP (4.4+/-0.5%). Infarct size was reduced in the ADO-CP (29+/-2%) and ADO-R (21+/-2%) groups compared with the BCP group (42+/-4%). Edema in the myocardial area at risk was decreased in the ADO-CP (82+/-0.2%) and ADO-R (80+/-0.4%) groups compared with the BCP group (86+/-0.7%). Adherence of fluorescently labeled neutrophils (PMNs) to postischemic coronary artery endothelium was attenuated by ADO-R (55+/-2 PMNs/mm(2)), but not by ADO-CP (114+/-5 PMNs/mm(2)), compared with BCP (118+/-3 PMNs/mm(2)).
The results show that BCP supplemented with ADO reduces infarct size, preserves postischemic systolic and diastolic regional function but does not attenuate coronary artery endothelial dysfunction unless administered during reperfusion.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>PMID: 10567333</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adenosine - administration & dosage ; Analgesics - administration & dosage ; Animals ; Biological and medical sciences ; Blood Pressure ; Cardiology. Vascular system ; Cardiopulmonary Bypass ; Coronary heart disease ; Dogs ; Heart ; Heart Arrest, Induced - methods ; Medical sciences ; Myocardial Reperfusion Injury - prevention & control ; Receptors, Purinergic P1</subject><ispartof>Circulation (New York, N.Y.), 1999-11, Vol.100 (19), p.II376-II383</ispartof><rights>2000 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Nov 9, 1999</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,23930,23931,25140</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1201356$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10567333$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>THOURANI, V. H</creatorcontrib><creatorcontrib>RONSON, R. S</creatorcontrib><creatorcontrib>VAN WYLEN, D. G. L</creatorcontrib><creatorcontrib>SHEARER, S. T</creatorcontrib><creatorcontrib>KATZMARK, S. L</creatorcontrib><creatorcontrib>ZHAO, Z.-Q</creatorcontrib><creatorcontrib>HAN, D. C</creatorcontrib><creatorcontrib>GUYTON, R. A</creatorcontrib><creatorcontrib>VINTEN-JOHANSEN, J</creatorcontrib><title>Adenosine-supplemented blood cardioplegia attenuates postischemic dysfunction after severe regional ischemia</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO's potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusion reduces postischemic dysfunction after severe regional ischemia.
After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4 degrees C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27 degrees C BCP was delivered for the terminal infusion. Dogs (n=6 per group) received unsupplemented BCP, ADO (100 micromol/L/L) supplemented in all infusions of BCP (ADO-CP), or ADO (100 micromol x L(-1) x L(-1)) supplemented only in the terminal infusion of BCP followed by intravenous ADO (140 microg x kg(-1) x min(-1)) infusion for the first 30 minutes of reperfusion (ADO-R). Postischemic regional systolic shortening was significantly greater in the ADO-R group (5+/-2.0%) than in the BCP group (-3+/-1.0%), but not in the ADO-CP group (2+/-0.2%). Postischemic regional diastolic stiffness in the area at risk during end reperfusion was lower with ADO-R (1.8+/-0.3%) than with ADO-CP (2.7+/-0.3%) or BCP (4.4+/-0.5%). Infarct size was reduced in the ADO-CP (29+/-2%) and ADO-R (21+/-2%) groups compared with the BCP group (42+/-4%). Edema in the myocardial area at risk was decreased in the ADO-CP (82+/-0.2%) and ADO-R (80+/-0.4%) groups compared with the BCP group (86+/-0.7%). Adherence of fluorescently labeled neutrophils (PMNs) to postischemic coronary artery endothelium was attenuated by ADO-R (55+/-2 PMNs/mm(2)), but not by ADO-CP (114+/-5 PMNs/mm(2)), compared with BCP (118+/-3 PMNs/mm(2)).
The results show that BCP supplemented with ADO reduces infarct size, preserves postischemic systolic and diastolic regional function but does not attenuate coronary artery endothelial dysfunction unless administered during reperfusion.</description><subject>Adenosine - administration & dosage</subject><subject>Analgesics - administration & dosage</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Cardiology. Vascular system</subject><subject>Cardiopulmonary Bypass</subject><subject>Coronary heart disease</subject><subject>Dogs</subject><subject>Heart</subject><subject>Heart Arrest, Induced - methods</subject><subject>Medical sciences</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Receptors, Purinergic P1</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0E1LxDAQBuAgiruu_gUJIt4KTdKmzXFZ_IIFL3ou02bidmmTmqSC_96AFcHTMMMzw_CekDUreZEVpVCnZJ3nucoqwfmKXIRwTK0UVXlOViwvZSWEWJNhq9G60FvMwjxNA45oI2raDs5p2oHXvUvT9x4oxIh2hoiBTi7EPnQHHPuO6q9gZtvF3lkKJqKnAT_RI_VpzVkY6ELhkpwZGAJeLXVD3h7uX3dP2f7l8Xm33WcHwUTMapNrKUTNsDJcM9WiVgZ0W2smRclBI7DKqIpDLUvQBloFyLFolSkqzIXYkLufu5N3HzOG2IzpBRwGsOjm0EjFFS9UleDNP3h0s08vh4YzniKSokjoekFzO6JuJt-P4L-a3xATuF0AhA4G48F2ffhzPGeilOIbTjp-qA</recordid><startdate>19991109</startdate><enddate>19991109</enddate><creator>THOURANI, V. H</creator><creator>RONSON, R. S</creator><creator>VAN WYLEN, D. G. L</creator><creator>SHEARER, S. T</creator><creator>KATZMARK, S. L</creator><creator>ZHAO, Z.-Q</creator><creator>HAN, D. C</creator><creator>GUYTON, R. A</creator><creator>VINTEN-JOHANSEN, J</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>19991109</creationdate><title>Adenosine-supplemented blood cardioplegia attenuates postischemic dysfunction after severe regional ischemia</title><author>THOURANI, V. H ; RONSON, R. S ; VAN WYLEN, D. G. L ; SHEARER, S. T ; KATZMARK, S. L ; ZHAO, Z.-Q ; HAN, D. C ; GUYTON, R. A ; VINTEN-JOHANSEN, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h313t-8f0d63381e7f2d19bed9fadb8d16352adea17f972a865adfab9ae2e4b9f47e033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adenosine - administration & dosage</topic><topic>Analgesics - administration & dosage</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Cardiology. Vascular system</topic><topic>Cardiopulmonary Bypass</topic><topic>Coronary heart disease</topic><topic>Dogs</topic><topic>Heart</topic><topic>Heart Arrest, Induced - methods</topic><topic>Medical sciences</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Receptors, Purinergic P1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>THOURANI, V. H</creatorcontrib><creatorcontrib>RONSON, R. S</creatorcontrib><creatorcontrib>VAN WYLEN, D. G. L</creatorcontrib><creatorcontrib>SHEARER, S. T</creatorcontrib><creatorcontrib>KATZMARK, S. L</creatorcontrib><creatorcontrib>ZHAO, Z.-Q</creatorcontrib><creatorcontrib>HAN, D. C</creatorcontrib><creatorcontrib>GUYTON, R. A</creatorcontrib><creatorcontrib>VINTEN-JOHANSEN, J</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>THOURANI, V. H</au><au>RONSON, R. S</au><au>VAN WYLEN, D. G. L</au><au>SHEARER, S. T</au><au>KATZMARK, S. L</au><au>ZHAO, Z.-Q</au><au>HAN, D. C</au><au>GUYTON, R. A</au><au>VINTEN-JOHANSEN, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adenosine-supplemented blood cardioplegia attenuates postischemic dysfunction after severe regional ischemia</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1999-11-09</date><risdate>1999</risdate><volume>100</volume><issue>19</issue><spage>II376</spage><epage>II383</epage><pages>II376-II383</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO's potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusion reduces postischemic dysfunction after severe regional ischemia.
After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4 degrees C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27 degrees C BCP was delivered for the terminal infusion. Dogs (n=6 per group) received unsupplemented BCP, ADO (100 micromol/L/L) supplemented in all infusions of BCP (ADO-CP), or ADO (100 micromol x L(-1) x L(-1)) supplemented only in the terminal infusion of BCP followed by intravenous ADO (140 microg x kg(-1) x min(-1)) infusion for the first 30 minutes of reperfusion (ADO-R). Postischemic regional systolic shortening was significantly greater in the ADO-R group (5+/-2.0%) than in the BCP group (-3+/-1.0%), but not in the ADO-CP group (2+/-0.2%). Postischemic regional diastolic stiffness in the area at risk during end reperfusion was lower with ADO-R (1.8+/-0.3%) than with ADO-CP (2.7+/-0.3%) or BCP (4.4+/-0.5%). Infarct size was reduced in the ADO-CP (29+/-2%) and ADO-R (21+/-2%) groups compared with the BCP group (42+/-4%). Edema in the myocardial area at risk was decreased in the ADO-CP (82+/-0.2%) and ADO-R (80+/-0.4%) groups compared with the BCP group (86+/-0.7%). Adherence of fluorescently labeled neutrophils (PMNs) to postischemic coronary artery endothelium was attenuated by ADO-R (55+/-2 PMNs/mm(2)), but not by ADO-CP (114+/-5 PMNs/mm(2)), compared with BCP (118+/-3 PMNs/mm(2)).
The results show that BCP supplemented with ADO reduces infarct size, preserves postischemic systolic and diastolic regional function but does not attenuate coronary artery endothelial dysfunction unless administered during reperfusion.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>10567333</pmid></addata></record> |
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| subjects | Adenosine - administration & dosage Analgesics - administration & dosage Animals Biological and medical sciences Blood Pressure Cardiology. Vascular system Cardiopulmonary Bypass Coronary heart disease Dogs Heart Heart Arrest, Induced - methods Medical sciences Myocardial Reperfusion Injury - prevention & control Receptors, Purinergic P1 |
| title | Adenosine-supplemented blood cardioplegia attenuates postischemic dysfunction after severe regional ischemia |
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