Protection by the Calcium Antagonist Tiapamil, Against Cardiac Lymphatic Enzyme Leakage and Arrhythmias in Canine Hearts During Reperfusion
We examined the effects of tiapamil, a Ca antagonist, on infarct size, lymphatic enzyme release, and arrhythmias in reperfused, ischemic canine hearts. Three-hour reperfusion of the left anterior descending coronary artery, which had been ligated for 3 h, significantly increased cardiac lymphatic re...
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| Veröffentlicht in: | Journal of cardiovascular pharmacology 1986-01, Vol.8 (1), p.90-98 |
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| creator | Matsuura, Akihiro Ishihara, Takafumi Nakamura, Kazuo Himori, Norio Nakamura, Keiji |
| description | We examined the effects of tiapamil, a Ca antagonist, on infarct size, lymphatic enzyme release, and arrhythmias in reperfused, ischemic canine hearts. Three-hour reperfusion of the left anterior descending coronary artery, which had been ligated for 3 h, significantly increased cardiac lymphatic release of lactate dehydrogenase (LDH), cathepsin D and creatine phosphokinase (CPK), and the incidence of ventricular premature contractions (VPCs), the increases being markedly higher than those in ligation period. Tiapamil, at the i.v. dose of 3 mg/kg/h for 6 h during the ligation and reperfusion periods markedly reduced these increases in lymphatic levels of LDH and cathepsin D and in VPCs, and significantly decreased infarct size. Tiapamil treatment only during the ligation period had similar preserving effects, but tiapamil treatment only during reperfusion did not. These results suggest that blockade of the Ca channel must be achieved during the early phase of an ischemic episode in order to prevent myocardial deterioration during reperfusion. |
| doi_str_mv | 10.1097/00005344-198601000-00015 |
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Three-hour reperfusion of the left anterior descending coronary artery, which had been ligated for 3 h, significantly increased cardiac lymphatic release of lactate dehydrogenase (LDH), cathepsin D and creatine phosphokinase (CPK), and the incidence of ventricular premature contractions (VPCs), the increases being markedly higher than those in ligation period. Tiapamil, at the i.v. dose of 3 mg/kg/h for 6 h during the ligation and reperfusion periods markedly reduced these increases in lymphatic levels of LDH and cathepsin D and in VPCs, and significantly decreased infarct size. Tiapamil treatment only during the ligation period had similar preserving effects, but tiapamil treatment only during reperfusion did not. These results suggest that blockade of the Ca channel must be achieved during the early phase of an ischemic episode in order to prevent myocardial deterioration during reperfusion.</description><identifier>ISSN: 0160-2446</identifier><identifier>EISSN: 1533-4023</identifier><identifier>DOI: 10.1097/00005344-198601000-00015</identifier><identifier>PMID: 2419700</identifier><identifier>CODEN: JCPCDT</identifier><language>eng</language><publisher>Philadelphia, PA: Lippincott-Raven Publishers</publisher><subject>Animals ; Antiarythmic agents ; Arrhythmias, Cardiac - etiology ; Arrhythmias, Cardiac - prevention & control ; Biological and medical sciences ; Calcium Channel Blockers - pharmacology ; Cardiovascular system ; Cathepsin D - metabolism ; Coronary Disease - drug therapy ; Coronary Disease - physiopathology ; Creatine Kinase - metabolism ; Dogs ; Female ; L-Lactate Dehydrogenase - metabolism ; Lymphatic System - drug effects ; Lymphatic System - enzymology ; Male ; Medical sciences ; Myocardial Infarction - drug therapy ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Pharmacology. Drug treatments ; Propylamines - administration & dosage ; Propylamines - pharmacology ; Tiapamil Hydrochloride ; Time Factors</subject><ispartof>Journal of cardiovascular pharmacology, 1986-01, Vol.8 (1), p.90-98</ispartof><rights>Lippincott-Raven Publishers.</rights><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00005344-198601000-00015$$EHTML$$P50$$Gwolterskluwer$$H</linktohtml><link.rule.ids>314,776,780,4010,4595,27900,27901,27902,65434</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8744770$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2419700$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsuura, Akihiro</creatorcontrib><creatorcontrib>Ishihara, Takafumi</creatorcontrib><creatorcontrib>Nakamura, Kazuo</creatorcontrib><creatorcontrib>Himori, Norio</creatorcontrib><creatorcontrib>Nakamura, Keiji</creatorcontrib><title>Protection by the Calcium Antagonist Tiapamil, Against Cardiac Lymphatic Enzyme Leakage and Arrhythmias in Canine Hearts During Reperfusion</title><title>Journal of cardiovascular pharmacology</title><addtitle>J Cardiovasc Pharmacol</addtitle><description>We examined the effects of tiapamil, a Ca antagonist, on infarct size, lymphatic enzyme release, and arrhythmias in reperfused, ischemic canine hearts. Three-hour reperfusion of the left anterior descending coronary artery, which had been ligated for 3 h, significantly increased cardiac lymphatic release of lactate dehydrogenase (LDH), cathepsin D and creatine phosphokinase (CPK), and the incidence of ventricular premature contractions (VPCs), the increases being markedly higher than those in ligation period. Tiapamil, at the i.v. dose of 3 mg/kg/h for 6 h during the ligation and reperfusion periods markedly reduced these increases in lymphatic levels of LDH and cathepsin D and in VPCs, and significantly decreased infarct size. Tiapamil treatment only during the ligation period had similar preserving effects, but tiapamil treatment only during reperfusion did not. These results suggest that blockade of the Ca channel must be achieved during the early phase of an ischemic episode in order to prevent myocardial deterioration during reperfusion.</description><subject>Animals</subject><subject>Antiarythmic agents</subject><subject>Arrhythmias, Cardiac - etiology</subject><subject>Arrhythmias, Cardiac - prevention & control</subject><subject>Biological and medical sciences</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Cardiovascular system</subject><subject>Cathepsin D - metabolism</subject><subject>Coronary Disease - drug therapy</subject><subject>Coronary Disease - physiopathology</subject><subject>Creatine Kinase - metabolism</subject><subject>Dogs</subject><subject>Female</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Lymphatic System - drug effects</subject><subject>Lymphatic System - enzymology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Propylamines - administration & dosage</subject><subject>Propylamines - pharmacology</subject><subject>Tiapamil Hydrochloride</subject><subject>Time Factors</subject><issn>0160-2446</issn><issn>1533-4023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFktGO1CAUhhujWcfVRzDhwnhlFQqFcjkZV9dkEo1Zr8mB0iluSyvQbOor-NIyzjh3RhJCOOf7DyfnpygQwW8JluIdzqumjJVENhyTfCvzJvWjYkNqSkuGK_q42GDCcVkxxp8Wz2L8nglWC35VXFWMSIHxpvj1JUzJmuQmj_SKUm_RDgbjlhFtfYLD5F1M6M7BDKMb3qDtAZzPkR2E1oFB-3Wce0jOoBv_cx0t2lu4h4NF4Fu0DaFfUz86iMj5rPHOW3RrIaSI3i_B-QP6amcbuiXmBp4XTzoYon1xPq-Lbx9u7na35f7zx0-77b40jOC6pNpIYjRISkyDG8G1rE2jecu01BVUkjVGdhwMCEKlsZxjMJRXnWai0bil18XrU905TD8WG5MaXTR2GMDbaYlKcJFHW7P_gnmadcXFEWxOoAlTjMF2ag5uhLAqgtXRMPXXMHUxTP0xLEtfnt9Y9Gjbi_DsUM6_OuchGhi6AN64eMEawZgQR4ydsIdpSDbE-2F5sEH1FobUq399F_obthKuQA</recordid><startdate>198601</startdate><enddate>198601</enddate><creator>Matsuura, Akihiro</creator><creator>Ishihara, Takafumi</creator><creator>Nakamura, Kazuo</creator><creator>Himori, Norio</creator><creator>Nakamura, Keiji</creator><general>Lippincott-Raven Publishers</general><general>Lippincott</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>7QP</scope><scope>7X8</scope></search><sort><creationdate>198601</creationdate><title>Protection by the Calcium Antagonist Tiapamil, Against Cardiac Lymphatic Enzyme Leakage and Arrhythmias in Canine Hearts During Reperfusion</title><author>Matsuura, Akihiro ; Ishihara, Takafumi ; Nakamura, Kazuo ; Himori, Norio ; Nakamura, Keiji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4105-3bc91cba931c80876b95c8b6d4b9b2a2948c9f6aca7139ce660ac362fb478b0d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Animals</topic><topic>Antiarythmic agents</topic><topic>Arrhythmias, Cardiac - etiology</topic><topic>Arrhythmias, Cardiac - prevention & control</topic><topic>Biological and medical sciences</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Cardiovascular system</topic><topic>Cathepsin D - metabolism</topic><topic>Coronary Disease - drug therapy</topic><topic>Coronary Disease - physiopathology</topic><topic>Creatine Kinase - metabolism</topic><topic>Dogs</topic><topic>Female</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Lymphatic System - drug effects</topic><topic>Lymphatic System - enzymology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Propylamines - administration & dosage</topic><topic>Propylamines - pharmacology</topic><topic>Tiapamil Hydrochloride</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsuura, Akihiro</creatorcontrib><creatorcontrib>Ishihara, Takafumi</creatorcontrib><creatorcontrib>Nakamura, Kazuo</creatorcontrib><creatorcontrib>Himori, Norio</creatorcontrib><creatorcontrib>Nakamura, Keiji</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>Calcium & Calcified Tissue Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cardiovascular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsuura, Akihiro</au><au>Ishihara, Takafumi</au><au>Nakamura, Kazuo</au><au>Himori, Norio</au><au>Nakamura, Keiji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protection by the Calcium Antagonist Tiapamil, Against Cardiac Lymphatic Enzyme Leakage and Arrhythmias in Canine Hearts During Reperfusion</atitle><jtitle>Journal of cardiovascular pharmacology</jtitle><addtitle>J Cardiovasc Pharmacol</addtitle><date>1986-01</date><risdate>1986</risdate><volume>8</volume><issue>1</issue><spage>90</spage><epage>98</epage><pages>90-98</pages><issn>0160-2446</issn><eissn>1533-4023</eissn><coden>JCPCDT</coden><abstract>We examined the effects of tiapamil, a Ca antagonist, on infarct size, lymphatic enzyme release, and arrhythmias in reperfused, ischemic canine hearts. Three-hour reperfusion of the left anterior descending coronary artery, which had been ligated for 3 h, significantly increased cardiac lymphatic release of lactate dehydrogenase (LDH), cathepsin D and creatine phosphokinase (CPK), and the incidence of ventricular premature contractions (VPCs), the increases being markedly higher than those in ligation period. Tiapamil, at the i.v. dose of 3 mg/kg/h for 6 h during the ligation and reperfusion periods markedly reduced these increases in lymphatic levels of LDH and cathepsin D and in VPCs, and significantly decreased infarct size. Tiapamil treatment only during the ligation period had similar preserving effects, but tiapamil treatment only during reperfusion did not. These results suggest that blockade of the Ca channel must be achieved during the early phase of an ischemic episode in order to prevent myocardial deterioration during reperfusion.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>Lippincott-Raven Publishers</pub><pmid>2419700</pmid><doi>10.1097/00005344-198601000-00015</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Journals@Ovid LWW Legacy Archive; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Animals Antiarythmic agents Arrhythmias, Cardiac - etiology Arrhythmias, Cardiac - prevention & control Biological and medical sciences Calcium Channel Blockers - pharmacology Cardiovascular system Cathepsin D - metabolism Coronary Disease - drug therapy Coronary Disease - physiopathology Creatine Kinase - metabolism Dogs Female L-Lactate Dehydrogenase - metabolism Lymphatic System - drug effects Lymphatic System - enzymology Male Medical sciences Myocardial Infarction - drug therapy Myocardial Infarction - pathology Myocardial Infarction - physiopathology Pharmacology. Drug treatments Propylamines - administration & dosage Propylamines - pharmacology Tiapamil Hydrochloride Time Factors |
| title | Protection by the Calcium Antagonist Tiapamil, Against Cardiac Lymphatic Enzyme Leakage and Arrhythmias in Canine Hearts During Reperfusion |
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