THE EFFECT OF MOLSIDOMINE ON INTRAMYOCARDIAL PRESSURE AND REGIONAL MYOCARDIAL BLOOD FLOW IN THE CANINE ISCHEMIC MYOCARDIUM
Molsidomine was administered intraduodenally to anesthetized dogs which were instrumented for measurements of aortic and left ventricular (LV) pressures, coronary perfusion pressure, intramyocardial pressure in the subendocardium, and subendocardial and subepicardial myocardial blood flow in the isc...
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| Veröffentlicht in: | JAPANESE CIRCULATION JOURNAL 1985/05/20, Vol.49(5), pp.507-515 |
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| container_title | JAPANESE CIRCULATION JOURNAL |
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| creator | KINOSHITA, MASAHIKO MASHIRO, IWAO MITSUNAMI, KENICHI FUKUHARA, TAKEHISA MOTOMURA, MASAKAZU BITO, KEIZO KAWAKITA, SEIICHI |
| description | Molsidomine was administered intraduodenally to anesthetized dogs which were instrumented for measurements of aortic and left ventricular (LV) pressures, coronary perfusion pressure, intramyocardial pressure in the subendocardium, and subendocardial and subepicardial myocardial blood flow in the ischemic and non-ischemic regions. The dogs were divided into two groups: group M (n=9) was administered molsidomine (0.2 mg/kg), group S (n=10), saline only. Maximum LV systolic pressure decline was 20% in group M and 3% in group S (p |
| doi_str_mv | 10.1253/jcj.49.507 |
| format | Article |
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The dogs were divided into two groups: group M (n=9) was administered molsidomine (0.2 mg/kg), group S (n=10), saline only. Maximum LV systolic pressure decline was 20% in group M and 3% in group S (p<0.05). Maximum LV end-diastolic pressure decline was 63% and 35% in groups M and S, respectively (p<0.05). There was no difference between mean aortic pressure and coronary perfusion pressure between the two groups. The subepicardial blood flow in the ischemic region was decreased (-23% in group M vs 5% in group S; p<0.05), but subendocardial blood flow in the ischemic region increased only slightly in group M. The ratio of subendocardial to subepicardial blood flow increased at 15 and 30 min after administration of molsidomine in the ischemic area (67% in group M vs -10% in group S; p<0.050. but did not show any change in the non-ischemic region. Intramyocardial pressure at systole did not show any change but it decreased at end-diastole, (-32% in group M vs -7% in group S; p<0.05). Thus molsidomine redistributed the myocardial blood flow from the subepicardium to the subendocardium and from the non-ischemic to the ischemic region. This redistribution was associated with a reduction in both LV end-diastolic pressure and intramyocardial pressure at end-diastole.</description><identifier>ISSN: 0047-1828</identifier><identifier>EISSN: 1347-4839</identifier><identifier>DOI: 10.1253/jcj.49.507</identifier><identifier>PMID: 3839541</identifier><identifier>CODEN: JCIRA2</identifier><language>eng</language><publisher>Kyoto: The Japanese Circulation Society</publisher><subject>Animals ; Antianginal agents. Coronary vasodilator agents ; Biological and medical sciences ; Blood Pressure - drug effects ; Cardiovascular system ; Coronary Circulation - drug effects ; Coronary Disease - physiopathology ; Dogs ; Heart - drug effects ; Intramyocardial pressure ; Kinetics ; Medical sciences ; Molsidomine ; Myocardial ischemia ; Oxadiazoles - pharmacology ; Pharmacology. Drug treatments ; Regional Blood Flow - drug effects ; Regional myocardial blood flow ; Sydnones - metabolism ; Sydnones - pharmacology</subject><ispartof>JAPANESE CIRCULATION JOURNAL, 1985/05/20, Vol.49(5), pp.507-515</ispartof><rights>Japanese Circulation Society</rights><rights>1985 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=9279069$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3839541$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KINOSHITA, MASAHIKO</creatorcontrib><creatorcontrib>MASHIRO, IWAO</creatorcontrib><creatorcontrib>MITSUNAMI, KENICHI</creatorcontrib><creatorcontrib>FUKUHARA, TAKEHISA</creatorcontrib><creatorcontrib>MOTOMURA, MASAKAZU</creatorcontrib><creatorcontrib>BITO, KEIZO</creatorcontrib><creatorcontrib>KAWAKITA, SEIICHI</creatorcontrib><title>THE EFFECT OF MOLSIDOMINE ON INTRAMYOCARDIAL PRESSURE AND REGIONAL MYOCARDIAL BLOOD FLOW IN THE CANINE ISCHEMIC MYOCARDIUM</title><title>JAPANESE CIRCULATION JOURNAL</title><addtitle>JAPANESE CIRCULATION JOURNAL</addtitle><description>Molsidomine was administered intraduodenally to anesthetized dogs which were instrumented for measurements of aortic and left ventricular (LV) pressures, coronary perfusion pressure, intramyocardial pressure in the subendocardium, and subendocardial and subepicardial myocardial blood flow in the ischemic and non-ischemic regions. The dogs were divided into two groups: group M (n=9) was administered molsidomine (0.2 mg/kg), group S (n=10), saline only. Maximum LV systolic pressure decline was 20% in group M and 3% in group S (p<0.05). Maximum LV end-diastolic pressure decline was 63% and 35% in groups M and S, respectively (p<0.05). There was no difference between mean aortic pressure and coronary perfusion pressure between the two groups. The subepicardial blood flow in the ischemic region was decreased (-23% in group M vs 5% in group S; p<0.05), but subendocardial blood flow in the ischemic region increased only slightly in group M. The ratio of subendocardial to subepicardial blood flow increased at 15 and 30 min after administration of molsidomine in the ischemic area (67% in group M vs -10% in group S; p<0.050. but did not show any change in the non-ischemic region. Intramyocardial pressure at systole did not show any change but it decreased at end-diastole, (-32% in group M vs -7% in group S; p<0.05). Thus molsidomine redistributed the myocardial blood flow from the subepicardium to the subendocardium and from the non-ischemic to the ischemic region. This redistribution was associated with a reduction in both LV end-diastolic pressure and intramyocardial pressure at end-diastole.</description><subject>Animals</subject><subject>Antianginal agents. Coronary vasodilator agents</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiovascular system</subject><subject>Coronary Circulation - drug effects</subject><subject>Coronary Disease - physiopathology</subject><subject>Dogs</subject><subject>Heart - drug effects</subject><subject>Intramyocardial pressure</subject><subject>Kinetics</subject><subject>Medical sciences</subject><subject>Molsidomine</subject><subject>Myocardial ischemia</subject><subject>Oxadiazoles - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Regional Blood Flow - drug effects</subject><subject>Regional myocardial blood flow</subject><subject>Sydnones - metabolism</subject><subject>Sydnones - pharmacology</subject><issn>0047-1828</issn><issn>1347-4839</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkEGP0zAQhS0EWsrChTuSD4gDUosd23FyDKmzjZTEKG2FOFmu60CitF3s9sD--nVpVbh4rHnfvNE8AN5jNMMRI18GM8xoOmOIvwATTCif0oSkL8EEofDHSZS8Bm-8HxCKOGXsDtyRoDOKJ-BptRBQFIXIV1AWsJbVspzLumwElA0sm1Wb1T9knrXzMqvgt1Ysl-tWwKyZw1Y8lLIJ3f-Ar5WUc1hU8nuYhWfvPGvOZuUyX4i6zG_wun4LXnV69Pbdtd6DdSFW-WJayYcyz6qpYTE9TjHtEk1Ti-K0ixg3nOstSgzGyWZLaZps4w6HamKGbGIpCpehjnOm4w3uyAaTe_Dp4vvoDr9P1h_VrvfGjqPe28PJKx5HEYkID-DnC2jcwXtnO_Xo-p12fxRG6hy0CkErmqoQdIA_XF1Pm53d3tBrskH_eNW1N3rsnN6b3t-wNOJpuChg4oIN_qh_2puu3bE3o1Wmd2bAaYz-7r08Yf0__Zd2yu7JM5ONkuw</recordid><startdate>19850101</startdate><enddate>19850101</enddate><creator>KINOSHITA, MASAHIKO</creator><creator>MASHIRO, IWAO</creator><creator>MITSUNAMI, KENICHI</creator><creator>FUKUHARA, TAKEHISA</creator><creator>MOTOMURA, MASAKAZU</creator><creator>BITO, KEIZO</creator><creator>KAWAKITA, SEIICHI</creator><general>The Japanese Circulation Society</general><general>Japanese Circulation Society</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>19850101</creationdate><title>THE EFFECT OF MOLSIDOMINE ON INTRAMYOCARDIAL PRESSURE AND REGIONAL MYOCARDIAL BLOOD FLOW IN THE CANINE ISCHEMIC MYOCARDIUM</title><author>KINOSHITA, MASAHIKO ; MASHIRO, IWAO ; MITSUNAMI, KENICHI ; FUKUHARA, TAKEHISA ; MOTOMURA, MASAKAZU ; BITO, KEIZO ; KAWAKITA, SEIICHI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c564t-14f8a49e069f257c77ad08c118bd4498d6f1449c650e8e408390f775a6b1f3b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Animals</topic><topic>Antianginal agents. Coronary vasodilator agents</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiovascular system</topic><topic>Coronary Circulation - drug effects</topic><topic>Coronary Disease - physiopathology</topic><topic>Dogs</topic><topic>Heart - drug effects</topic><topic>Intramyocardial pressure</topic><topic>Kinetics</topic><topic>Medical sciences</topic><topic>Molsidomine</topic><topic>Myocardial ischemia</topic><topic>Oxadiazoles - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Regional Blood Flow - drug effects</topic><topic>Regional myocardial blood flow</topic><topic>Sydnones - metabolism</topic><topic>Sydnones - pharmacology</topic><toplevel>online_resources</toplevel><creatorcontrib>KINOSHITA, MASAHIKO</creatorcontrib><creatorcontrib>MASHIRO, IWAO</creatorcontrib><creatorcontrib>MITSUNAMI, KENICHI</creatorcontrib><creatorcontrib>FUKUHARA, TAKEHISA</creatorcontrib><creatorcontrib>MOTOMURA, MASAKAZU</creatorcontrib><creatorcontrib>BITO, KEIZO</creatorcontrib><creatorcontrib>KAWAKITA, SEIICHI</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>JAPANESE CIRCULATION JOURNAL</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KINOSHITA, MASAHIKO</au><au>MASHIRO, IWAO</au><au>MITSUNAMI, KENICHI</au><au>FUKUHARA, TAKEHISA</au><au>MOTOMURA, MASAKAZU</au><au>BITO, KEIZO</au><au>KAWAKITA, SEIICHI</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>THE EFFECT OF MOLSIDOMINE ON INTRAMYOCARDIAL PRESSURE AND REGIONAL MYOCARDIAL BLOOD FLOW IN THE CANINE ISCHEMIC MYOCARDIUM</atitle><jtitle>JAPANESE CIRCULATION JOURNAL</jtitle><addtitle>JAPANESE CIRCULATION JOURNAL</addtitle><date>1985-01-01</date><risdate>1985</risdate><volume>49</volume><issue>5</issue><spage>507</spage><epage>515</epage><pages>507-515</pages><issn>0047-1828</issn><eissn>1347-4839</eissn><coden>JCIRA2</coden><abstract>Molsidomine was administered intraduodenally to anesthetized dogs which were instrumented for measurements of aortic and left ventricular (LV) pressures, coronary perfusion pressure, intramyocardial pressure in the subendocardium, and subendocardial and subepicardial myocardial blood flow in the ischemic and non-ischemic regions. The dogs were divided into two groups: group M (n=9) was administered molsidomine (0.2 mg/kg), group S (n=10), saline only. Maximum LV systolic pressure decline was 20% in group M and 3% in group S (p<0.05). Maximum LV end-diastolic pressure decline was 63% and 35% in groups M and S, respectively (p<0.05). There was no difference between mean aortic pressure and coronary perfusion pressure between the two groups. The subepicardial blood flow in the ischemic region was decreased (-23% in group M vs 5% in group S; p<0.05), but subendocardial blood flow in the ischemic region increased only slightly in group M. The ratio of subendocardial to subepicardial blood flow increased at 15 and 30 min after administration of molsidomine in the ischemic area (67% in group M vs -10% in group S; p<0.050. but did not show any change in the non-ischemic region. Intramyocardial pressure at systole did not show any change but it decreased at end-diastole, (-32% in group M vs -7% in group S; p<0.05). Thus molsidomine redistributed the myocardial blood flow from the subepicardium to the subendocardium and from the non-ischemic to the ischemic region. This redistribution was associated with a reduction in both LV end-diastolic pressure and intramyocardial pressure at end-diastole.</abstract><cop>Kyoto</cop><pub>The Japanese Circulation Society</pub><pmid>3839541</pmid><doi>10.1253/jcj.49.507</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0047-1828 |
| ispartof | JAPANESE CIRCULATION JOURNAL, 1985/05/20, Vol.49(5), pp.507-515 |
| issn | 0047-1828 1347-4839 |
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| subjects | Animals Antianginal agents. Coronary vasodilator agents Biological and medical sciences Blood Pressure - drug effects Cardiovascular system Coronary Circulation - drug effects Coronary Disease - physiopathology Dogs Heart - drug effects Intramyocardial pressure Kinetics Medical sciences Molsidomine Myocardial ischemia Oxadiazoles - pharmacology Pharmacology. Drug treatments Regional Blood Flow - drug effects Regional myocardial blood flow Sydnones - metabolism Sydnones - pharmacology |
| title | THE EFFECT OF MOLSIDOMINE ON INTRAMYOCARDIAL PRESSURE AND REGIONAL MYOCARDIAL BLOOD FLOW IN THE CANINE ISCHEMIC MYOCARDIUM |
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