Normothermic cardioplegia prevents intracellular calcium accumulation during cardioplegic arrest and reperfusion
Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion. We studied the effects of different temperatures during continuously perfused cardioplegic arrest on the changes of intracellular calcium concentration ([Ca2+]i) level in isol...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1994-11, Vol.90 (5 Pt 2), p.II316-II320 |
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| creator | Liu, X Engelman, R M Rousou, J A Flack, 3rd, J E Deaton, D W Das, D K |
| description | Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion. We studied the effects of different temperatures during continuously perfused cardioplegic arrest on the changes of intracellular calcium concentration ([Ca2+]i) level in isolated rat hearts.
Rat hearts were perfused by the Langendorff technique with Krebs-Henseleit bicarbonate (KHB) buffer. The [Ca2+]i was monitored by loading the heart with fura-2 acetoxymethyl ester and by using a [Ca2+]i analyzer. [Ca2+]i was calculated by determining the maximal and minimal fluorescent intensity for each heart. The hearts (n = 6 in each group) were subjected to cardioplegic arrest by continuous perfusion of oxygenated crystalloid K+ (15 mEq/L) cardioplegic solution (CPS) at different temperatures (4 degrees C, 20 degrees C, 28 degrees C, 37 degrees C) for 120 minutes, followed by 30 minutes of normothermic KHB buffer reperfusion. A fifth group received continuous perfusion as a control with 37 degrees C KHB buffer. The baseline values of [Ca2+]i were comparable in all experimental groups. In hearts perfused with 4 degrees C CPS, [Ca2+]i increased significantly during reperfusion (from 221 +/- 24 nmol/L [mean +/- SEM] at baseline to 341 +/- 19 at the end of reperfusion, P < .05). CPS perfusion at 20 degrees C also induced significant Ca2+ overloading during reperfusion, but not as much as in the 4 degrees C group. No significant [Ca2+]i increase occurred at 28 degrees C or 37 degrees C.
Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+ overloading during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion prevents the development of Ca2+ accumulation. These results provide experimental evidence for a detrimental effect of prolonged hypothermic continuous cardioplegia. |
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Rat hearts were perfused by the Langendorff technique with Krebs-Henseleit bicarbonate (KHB) buffer. The [Ca2+]i was monitored by loading the heart with fura-2 acetoxymethyl ester and by using a [Ca2+]i analyzer. [Ca2+]i was calculated by determining the maximal and minimal fluorescent intensity for each heart. The hearts (n = 6 in each group) were subjected to cardioplegic arrest by continuous perfusion of oxygenated crystalloid K+ (15 mEq/L) cardioplegic solution (CPS) at different temperatures (4 degrees C, 20 degrees C, 28 degrees C, 37 degrees C) for 120 minutes, followed by 30 minutes of normothermic KHB buffer reperfusion. A fifth group received continuous perfusion as a control with 37 degrees C KHB buffer. The baseline values of [Ca2+]i were comparable in all experimental groups. In hearts perfused with 4 degrees C CPS, [Ca2+]i increased significantly during reperfusion (from 221 +/- 24 nmol/L [mean +/- SEM] at baseline to 341 +/- 19 at the end of reperfusion, P < .05). CPS perfusion at 20 degrees C also induced significant Ca2+ overloading during reperfusion, but not as much as in the 4 degrees C group. No significant [Ca2+]i increase occurred at 28 degrees C or 37 degrees C.
Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+ overloading during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion prevents the development of Ca2+ accumulation. These results provide experimental evidence for a detrimental effect of prolonged hypothermic continuous cardioplegia.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>PMID: 7955273</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Animals ; Calcium - metabolism ; Cardioplegic Solutions ; Heart Arrest, Induced - methods ; Hypothermia, Induced ; Male ; Myocardial Reperfusion ; Myocardial Reperfusion Injury - etiology ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - prevention & control ; Myocardium - metabolism ; Perfusion ; Rats ; Rats, Sprague-Dawley ; Temperature ; Time Factors</subject><ispartof>Circulation (New York, N.Y.), 1994-11, Vol.90 (5 Pt 2), p.II316-II320</ispartof><rights>Copyright American Heart Association, Inc. Nov 1994</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7955273$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, X</creatorcontrib><creatorcontrib>Engelman, R M</creatorcontrib><creatorcontrib>Rousou, J A</creatorcontrib><creatorcontrib>Flack, 3rd, J E</creatorcontrib><creatorcontrib>Deaton, D W</creatorcontrib><creatorcontrib>Das, D K</creatorcontrib><title>Normothermic cardioplegia prevents intracellular calcium accumulation during cardioplegic arrest and reperfusion</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion. We studied the effects of different temperatures during continuously perfused cardioplegic arrest on the changes of intracellular calcium concentration ([Ca2+]i) level in isolated rat hearts.
Rat hearts were perfused by the Langendorff technique with Krebs-Henseleit bicarbonate (KHB) buffer. The [Ca2+]i was monitored by loading the heart with fura-2 acetoxymethyl ester and by using a [Ca2+]i analyzer. [Ca2+]i was calculated by determining the maximal and minimal fluorescent intensity for each heart. The hearts (n = 6 in each group) were subjected to cardioplegic arrest by continuous perfusion of oxygenated crystalloid K+ (15 mEq/L) cardioplegic solution (CPS) at different temperatures (4 degrees C, 20 degrees C, 28 degrees C, 37 degrees C) for 120 minutes, followed by 30 minutes of normothermic KHB buffer reperfusion. A fifth group received continuous perfusion as a control with 37 degrees C KHB buffer. The baseline values of [Ca2+]i were comparable in all experimental groups. In hearts perfused with 4 degrees C CPS, [Ca2+]i increased significantly during reperfusion (from 221 +/- 24 nmol/L [mean +/- SEM] at baseline to 341 +/- 19 at the end of reperfusion, P < .05). CPS perfusion at 20 degrees C also induced significant Ca2+ overloading during reperfusion, but not as much as in the 4 degrees C group. No significant [Ca2+]i increase occurred at 28 degrees C or 37 degrees C.
Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+ overloading during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion prevents the development of Ca2+ accumulation. These results provide experimental evidence for a detrimental effect of prolonged hypothermic continuous cardioplegia.</description><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Cardioplegic Solutions</subject><subject>Heart Arrest, Induced - methods</subject><subject>Hypothermia, Induced</subject><subject>Male</subject><subject>Myocardial Reperfusion</subject><subject>Myocardial Reperfusion Injury - etiology</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Myocardium - metabolism</subject><subject>Perfusion</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Temperature</subject><subject>Time Factors</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE1LAzEQhoMotVZ_ghA8eFvIx2azOUpRKxS96HnJJtOasl9ONoL_3og9iKfhfXlm5p05IUuuRFmUSppTsmSMmUJLIc7JRYyHLCup1YIstFFKaLkk0_OI_Ti_A_bBUWfRh3HqYB8snRA-YZgjDcOM1kHXpc5iZjoXUk-tc6nPzhzGgfqEYdj_7XfUIkKcqR08RZgAdylm9JKc7WwX4epYV-Tt4f51vSm2L49P67ttMQmp5qLMWVuhvHO8rjiIrLw1sq61N7p0THOvW8OcypaqwRhVtcBK4KWvyp2t5Yrc_s6dcPxIOUjTh_hzhB1gTLHRVZ0XcZPBm3_gYUw45GyN4EIzVvMqQ9dHKLU9-GbC0Fv8ao5_lN9_hXGv</recordid><startdate>199411</startdate><enddate>199411</enddate><creator>Liu, X</creator><creator>Engelman, R M</creator><creator>Rousou, J A</creator><creator>Flack, 3rd, J E</creator><creator>Deaton, D W</creator><creator>Das, D K</creator><general>American Heart Association, Inc</general><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>199411</creationdate><title>Normothermic cardioplegia prevents intracellular calcium accumulation during cardioplegic arrest and reperfusion</title><author>Liu, X ; Engelman, R M ; Rousou, J A ; Flack, 3rd, J E ; Deaton, D W ; Das, D K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p235t-4000b25dcc1861e200bda93887d974c071d7b90c538858e9956be04e14d64fa83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>Calcium - metabolism</topic><topic>Cardioplegic Solutions</topic><topic>Heart Arrest, Induced - methods</topic><topic>Hypothermia, Induced</topic><topic>Male</topic><topic>Myocardial Reperfusion</topic><topic>Myocardial Reperfusion Injury - etiology</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Myocardium - metabolism</topic><topic>Perfusion</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Temperature</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, X</creatorcontrib><creatorcontrib>Engelman, R M</creatorcontrib><creatorcontrib>Rousou, J A</creatorcontrib><creatorcontrib>Flack, 3rd, J E</creatorcontrib><creatorcontrib>Deaton, D W</creatorcontrib><creatorcontrib>Das, D K</creatorcontrib><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>Liu, X</au><au>Engelman, R M</au><au>Rousou, J A</au><au>Flack, 3rd, J E</au><au>Deaton, D W</au><au>Das, D K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Normothermic cardioplegia prevents intracellular calcium accumulation during cardioplegic arrest and reperfusion</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1994-11</date><risdate>1994</risdate><volume>90</volume><issue>5 Pt 2</issue><spage>II316</spage><epage>II320</epage><pages>II316-II320</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion. We studied the effects of different temperatures during continuously perfused cardioplegic arrest on the changes of intracellular calcium concentration ([Ca2+]i) level in isolated rat hearts.
Rat hearts were perfused by the Langendorff technique with Krebs-Henseleit bicarbonate (KHB) buffer. The [Ca2+]i was monitored by loading the heart with fura-2 acetoxymethyl ester and by using a [Ca2+]i analyzer. [Ca2+]i was calculated by determining the maximal and minimal fluorescent intensity for each heart. The hearts (n = 6 in each group) were subjected to cardioplegic arrest by continuous perfusion of oxygenated crystalloid K+ (15 mEq/L) cardioplegic solution (CPS) at different temperatures (4 degrees C, 20 degrees C, 28 degrees C, 37 degrees C) for 120 minutes, followed by 30 minutes of normothermic KHB buffer reperfusion. A fifth group received continuous perfusion as a control with 37 degrees C KHB buffer. The baseline values of [Ca2+]i were comparable in all experimental groups. In hearts perfused with 4 degrees C CPS, [Ca2+]i increased significantly during reperfusion (from 221 +/- 24 nmol/L [mean +/- SEM] at baseline to 341 +/- 19 at the end of reperfusion, P < .05). CPS perfusion at 20 degrees C also induced significant Ca2+ overloading during reperfusion, but not as much as in the 4 degrees C group. No significant [Ca2+]i increase occurred at 28 degrees C or 37 degrees C.
Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+ overloading during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion prevents the development of Ca2+ accumulation. These results provide experimental evidence for a detrimental effect of prolonged hypothermic continuous cardioplegia.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>7955273</pmid></addata></record> |
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| subjects | Animals Calcium - metabolism Cardioplegic Solutions Heart Arrest, Induced - methods Hypothermia, Induced Male Myocardial Reperfusion Myocardial Reperfusion Injury - etiology Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - prevention & control Myocardium - metabolism Perfusion Rats Rats, Sprague-Dawley Temperature Time Factors |
| title | Normothermic cardioplegia prevents intracellular calcium accumulation during cardioplegic arrest and reperfusion |
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