Cellular mechanisms of ischemia-reperfusion injury
As of yet, only a few strategies to prevent myocardial reperfusion injury have been tested clinically. In the first minutes of reperfusion, the myocardium can be damaged by contracture development, causing mechanical stiffness, tissue necrosis, and the “stone heart” phenomenon. Reperfusion-induced c...
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| Veröffentlicht in: | The Annals of thoracic surgery 2003-02, Vol.75 (2), p.S644-S648 |
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| container_title | The Annals of thoracic surgery |
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| creator | Piper, H.Michael Meuter, Karsten Schäfer, Claudia |
| description | As of yet, only a few strategies to prevent myocardial reperfusion injury have been tested clinically. In the first minutes of reperfusion, the myocardium can be damaged by contracture development, causing mechanical stiffness, tissue necrosis, and the “stone heart” phenomenon. Reperfusion-induced contracture can have two different causes, namely, Ca
2+overload–induced contracture or rigor-type contracture. Ca
2+ contracture results from rapid re-energization of contractile cells with a persistent Ca
2+ overload. Strategies to prevent this type of injury are directed at cytosolic Ca
2+ control or myofibrillar Ca
2+ sensitivity. Rigor-contracture occurs when re-energization proceeds very slowly. It does not depend on Ca
2+ overload. It may be prevented by strategies improving early mitochondrial reactivation |
| doi_str_mv | 10.1016/S0003-4975(02)04686-6 |
| format | Article |
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2+overload–induced contracture or rigor-type contracture. Ca
2+ contracture results from rapid re-energization of contractile cells with a persistent Ca
2+ overload. Strategies to prevent this type of injury are directed at cytosolic Ca
2+ control or myofibrillar Ca
2+ sensitivity. Rigor-contracture occurs when re-energization proceeds very slowly. It does not depend on Ca
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2+overload–induced contracture or rigor-type contracture. Ca
2+ contracture results from rapid re-energization of contractile cells with a persistent Ca
2+ overload. Strategies to prevent this type of injury are directed at cytosolic Ca
2+ control or myofibrillar Ca
2+ sensitivity. Rigor-contracture occurs when re-energization proceeds very slowly. It does not depend on Ca
2+ overload. It may be prevented by strategies improving early mitochondrial reactivation</description><subject>Adenosine Triphosphate - analysis</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Cytosol - physiology</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Heart</subject><subject>Heart - physiopathology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mitochondria, Heart - physiology</subject><subject>Myocardial Contraction - physiology</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Myocardium - chemistry</subject><subject>Myocardium - cytology</subject><subject>Myocardium - pathology</subject><subject>Sarcolemma - physiology</subject><subject>Sodium-Calcium Exchanger - physiology</subject><issn>0003-4975</issn><issn>1552-6259</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LAzEQhoMoWj9-gtKLoofV2aSZ7J5Eil8geFDPIZud0JT9qElX6L83tUWPnoZhnpl5eRg7zeE6hxxv3gBAZJNSyUvgVzDBAjPcYaNcSp4hl-UuG_0iB-wwxnlqeRrvs4OcIygFOGJ8Sk0zNCaMW7Iz0_nYxnHvxj7aGbXeZIEWFNwQfd-NfTcfwuqY7TnTRDrZ1iP28XD_Pn3KXl4fn6d3L5mVHJeZzU1ZI3fADVRIhanqqkLBsbCilM5VVqG0skCBwsmyNhKcM2pSk1ROFEYcsYvN3UXoPweKS92mVCmu6agfolYCZK4QEig3oA19jIGcXgTfmrDSOei1LP0jS69NaOD6R5bGtHe2fTBULdV_W1s7CTjfAiZa07hgOuvjHzeRQgEvEne74Sjp-PIUdLSeOku1D2SXuu79P1G-AVmNhi8</recordid><startdate>20030201</startdate><enddate>20030201</enddate><creator>Piper, H.Michael</creator><creator>Meuter, Karsten</creator><creator>Schäfer, Claudia</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>20030201</creationdate><title>Cellular mechanisms of ischemia-reperfusion injury</title><author>Piper, H.Michael ; Meuter, Karsten ; Schäfer, Claudia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-c1a9d62f02a0b6e8abdbb63268c395ffbc765c586363f59da50ffa74de57f38a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adenosine Triphosphate - analysis</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Cytosol - physiology</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Heart</topic><topic>Heart - physiopathology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mitochondria, Heart - physiology</topic><topic>Myocardial Contraction - physiology</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardial Reperfusion Injury - physiopathology</topic><topic>Myocardium - chemistry</topic><topic>Myocardium - cytology</topic><topic>Myocardium - pathology</topic><topic>Sarcolemma - physiology</topic><topic>Sodium-Calcium Exchanger - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Piper, H.Michael</creatorcontrib><creatorcontrib>Meuter, Karsten</creatorcontrib><creatorcontrib>Schäfer, Claudia</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>Piper, H.Michael</au><au>Meuter, Karsten</au><au>Schäfer, Claudia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cellular mechanisms of ischemia-reperfusion injury</atitle><jtitle>The Annals of thoracic surgery</jtitle><addtitle>Ann Thorac Surg</addtitle><date>2003-02-01</date><risdate>2003</risdate><volume>75</volume><issue>2</issue><spage>S644</spage><epage>S648</epage><pages>S644-S648</pages><issn>0003-4975</issn><eissn>1552-6259</eissn><coden>ATHSAK</coden><abstract>As of yet, only a few strategies to prevent myocardial reperfusion injury have been tested clinically. In the first minutes of reperfusion, the myocardium can be damaged by contracture development, causing mechanical stiffness, tissue necrosis, and the “stone heart” phenomenon. Reperfusion-induced contracture can have two different causes, namely, Ca
2+overload–induced contracture or rigor-type contracture. Ca
2+ contracture results from rapid re-energization of contractile cells with a persistent Ca
2+ overload. Strategies to prevent this type of injury are directed at cytosolic Ca
2+ control or myofibrillar Ca
2+ sensitivity. Rigor-contracture occurs when re-energization proceeds very slowly. It does not depend on Ca
2+ overload. It may be prevented by strategies improving early mitochondrial reactivation</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>12607706</pmid><doi>10.1016/S0003-4975(02)04686-6</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adenosine Triphosphate - analysis Biological and medical sciences Cardiology. Vascular system Coronary heart disease Cytosol - physiology Endothelium, Vascular - physiopathology Heart Heart - physiopathology Humans Medical sciences Mitochondria, Heart - physiology Myocardial Contraction - physiology Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - physiopathology Myocardium - chemistry Myocardium - cytology Myocardium - pathology Sarcolemma - physiology Sodium-Calcium Exchanger - physiology |
| title | Cellular mechanisms of ischemia-reperfusion injury |
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