Enhancement of Endothelial Function Inhibits Left Atrial Thrombi Development in an Animal Model of Spontaneous Left Atrial Thrombosis
Background:Left atrial (LA) thrombosis is an important cause of systemic embolization. The SPORTS rat model of LA thrombi (Spontaneously-Running Tokushima-Shikoku), which have a unique characteristic of high voluntary wheel running, was previously established. The aim of the present study was to inv...
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| Veröffentlicht in: | Circulation Journal 2014/07/25, Vol.78(8), pp.1980-1988 |
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| container_end_page | 1988 |
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| container_issue | 8 |
| container_start_page | 1980 |
| container_title | Circulation Journal |
| container_volume | 78 |
| creator | Mawatari, Kazuaki Yoshioka, Emiko Toda, Satomi Yasui, Sonoko Furukawa, Hiroko Shimohata, Takaaki Ohnishi, Takamasa Morishima, Masaki Harada, Nagakatsu Takahashi, Akira Sakaue, Hiroshi Nakaya, Yutaka |
| description | Background:Left atrial (LA) thrombosis is an important cause of systemic embolization. The SPORTS rat model of LA thrombi (Spontaneously-Running Tokushima-Shikoku), which have a unique characteristic of high voluntary wheel running, was previously established. The aim of the present study was to investigate how SPORTS rats develop LA thrombi.Methods and Results:Nitric oxide (NO) produced from cardiovascular endothelial cells plays an important protective role in the local regulation of blood flow, vascular tone, and platelet aggregation. No evidence of atrial fibrillation or hypercoagulability in SPORTS rats regardless of age was found; however, SPORTS rats demonstrated endothelial dysfunction and a decrease of NO production from a young age. In addition, endothelial NO synthase activity was significantly decreased in the LA and thoracic aorta endothelia of SPORTS rats. While voluntary wheel running was able to intermittently increase NO levels, running did not statistically decrease the incidence of LA thrombi at autopsy. However, L-arginine treatment significantly increased NO production and provided protection from the development of LA thrombi in SPORTS rats.Conclusions:They present study results indicate that NO has an important role in the development of LA thrombus, and endothelia pathways could provide new targets of therapy to prevent LA thrombosis. (Circ J 2014; 78: 1980–1988) |
| doi_str_mv | 10.1253/circj.CJ-13-1398 |
| format | Article |
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The SPORTS rat model of LA thrombi (Spontaneously-Running Tokushima-Shikoku), which have a unique characteristic of high voluntary wheel running, was previously established. The aim of the present study was to investigate how SPORTS rats develop LA thrombi.Methods and Results:Nitric oxide (NO) produced from cardiovascular endothelial cells plays an important protective role in the local regulation of blood flow, vascular tone, and platelet aggregation. No evidence of atrial fibrillation or hypercoagulability in SPORTS rats regardless of age was found; however, SPORTS rats demonstrated endothelial dysfunction and a decrease of NO production from a young age. In addition, endothelial NO synthase activity was significantly decreased in the LA and thoracic aorta endothelia of SPORTS rats. While voluntary wheel running was able to intermittently increase NO levels, running did not statistically decrease the incidence of LA thrombi at autopsy. However, L-arginine treatment significantly increased NO production and provided protection from the development of LA thrombi in SPORTS rats.Conclusions:They present study results indicate that NO has an important role in the development of LA thrombus, and endothelia pathways could provide new targets of therapy to prevent LA thrombosis. (Circ J 2014; 78: 1980–1988)</description><identifier>ISSN: 1346-9843</identifier><identifier>EISSN: 1347-4820</identifier><identifier>DOI: 10.1253/circj.CJ-13-1398</identifier><identifier>PMID: 24859498</identifier><language>eng</language><publisher>Japan: The Japanese Circulation Society</publisher><subject>Animals ; Atrial fibrillation ; Disease Models, Animal ; Endothelial dysfunction ; Endothelium - metabolism ; Endothelium - pathology ; Female ; Heart Atria - metabolism ; Male ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Rats ; Thrombosis ; Thrombosis - metabolism ; Thrombosis - pathology ; Vasodilation</subject><ispartof>Circulation Journal, 2014/07/25, Vol.78(8), pp.1980-1988</ispartof><rights>2014 2013 THE JAPANESE CIRCULATION SOCIETY</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c622t-e35ec4996fb1b45c5afaab4cda828747646f77707abd44c17bd27d8a652646f53</citedby><cites>FETCH-LOGICAL-c622t-e35ec4996fb1b45c5afaab4cda828747646f77707abd44c17bd27d8a652646f53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1881,4014,27914,27915,27916</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24859498$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mawatari, Kazuaki</creatorcontrib><creatorcontrib>Yoshioka, Emiko</creatorcontrib><creatorcontrib>Toda, Satomi</creatorcontrib><creatorcontrib>Yasui, Sonoko</creatorcontrib><creatorcontrib>Furukawa, Hiroko</creatorcontrib><creatorcontrib>Shimohata, Takaaki</creatorcontrib><creatorcontrib>Ohnishi, Takamasa</creatorcontrib><creatorcontrib>Morishima, Masaki</creatorcontrib><creatorcontrib>Harada, Nagakatsu</creatorcontrib><creatorcontrib>Takahashi, Akira</creatorcontrib><creatorcontrib>Sakaue, Hiroshi</creatorcontrib><creatorcontrib>Nakaya, Yutaka</creatorcontrib><title>Enhancement of Endothelial Function Inhibits Left Atrial Thrombi Development in an Animal Model of Spontaneous Left Atrial Thrombosis</title><title>Circulation Journal</title><addtitle>Circ J</addtitle><description>Background:Left atrial (LA) thrombosis is an important cause of systemic embolization. The SPORTS rat model of LA thrombi (Spontaneously-Running Tokushima-Shikoku), which have a unique characteristic of high voluntary wheel running, was previously established. The aim of the present study was to investigate how SPORTS rats develop LA thrombi.Methods and Results:Nitric oxide (NO) produced from cardiovascular endothelial cells plays an important protective role in the local regulation of blood flow, vascular tone, and platelet aggregation. No evidence of atrial fibrillation or hypercoagulability in SPORTS rats regardless of age was found; however, SPORTS rats demonstrated endothelial dysfunction and a decrease of NO production from a young age. In addition, endothelial NO synthase activity was significantly decreased in the LA and thoracic aorta endothelia of SPORTS rats. While voluntary wheel running was able to intermittently increase NO levels, running did not statistically decrease the incidence of LA thrombi at autopsy. However, L-arginine treatment significantly increased NO production and provided protection from the development of LA thrombi in SPORTS rats.Conclusions:They present study results indicate that NO has an important role in the development of LA thrombus, and endothelia pathways could provide new targets of therapy to prevent LA thrombosis. (Circ J 2014; 78: 1980–1988)</description><subject>Animals</subject><subject>Atrial fibrillation</subject><subject>Disease Models, Animal</subject><subject>Endothelial dysfunction</subject><subject>Endothelium - metabolism</subject><subject>Endothelium - pathology</subject><subject>Female</subject><subject>Heart Atria - metabolism</subject><subject>Male</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Rats</subject><subject>Thrombosis</subject><subject>Thrombosis - metabolism</subject><subject>Thrombosis - pathology</subject><subject>Vasodilation</subject><issn>1346-9843</issn><issn>1347-4820</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkE2P0zAQhi0EYpeFOyfkI5cs8VdsH6vSwq6KOLCcLceZEFeJXWwXiR_A_yZpy-4FyRpbmmceeV6E3pL6llDBPjif3P52fV8RNh-tnqFrwrisuKL189O7qbTi7Aq9ynlf11TXQr9EV5QroblW1-jPJgw2OJggFBx7vAldLAOM3o54ewyu-BjwXRh860vGO-gLXpW0dB-GFKfW44_wC8Z4OAl8wDbgVfDTDHyJHYyL89shhmIDxOP_DDH7_Bq96O2Y4c3lvkHft5uH9edq9_XT3Xq1q1xDaamACXBc66ZvScuFE7a3tuWus4oqyWXDm15KWUvbdpw7ItuOyk7ZRtClJdgNen_2HlL8eYRczOSzg3E8_84QwXXDmGr4jNZn1KWYc4LeHNK8VvptSG2W8M0pfLO-N4SZJfx55N3Ffmwn6B4H_qU9A9szsM_F_oBHwKbi3QgXo1RGLeXJ_AQMNhkI7C_5CpyK</recordid><startdate>2014</startdate><enddate>2014</enddate><creator>Mawatari, Kazuaki</creator><creator>Yoshioka, Emiko</creator><creator>Toda, Satomi</creator><creator>Yasui, Sonoko</creator><creator>Furukawa, Hiroko</creator><creator>Shimohata, Takaaki</creator><creator>Ohnishi, Takamasa</creator><creator>Morishima, Masaki</creator><creator>Harada, Nagakatsu</creator><creator>Takahashi, Akira</creator><creator>Sakaue, Hiroshi</creator><creator>Nakaya, Yutaka</creator><general>The Japanese Circulation Society</general><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>2014</creationdate><title>Enhancement of Endothelial Function Inhibits Left Atrial Thrombi Development in an Animal Model of Spontaneous Left Atrial Thrombosis</title><author>Mawatari, Kazuaki ; Yoshioka, Emiko ; Toda, Satomi ; Yasui, Sonoko ; Furukawa, Hiroko ; Shimohata, Takaaki ; Ohnishi, Takamasa ; Morishima, Masaki ; Harada, Nagakatsu ; Takahashi, Akira ; Sakaue, Hiroshi ; Nakaya, Yutaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c622t-e35ec4996fb1b45c5afaab4cda828747646f77707abd44c17bd27d8a652646f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Atrial fibrillation</topic><topic>Disease Models, Animal</topic><topic>Endothelial dysfunction</topic><topic>Endothelium - metabolism</topic><topic>Endothelium - pathology</topic><topic>Female</topic><topic>Heart Atria - metabolism</topic><topic>Male</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Rats</topic><topic>Thrombosis</topic><topic>Thrombosis - metabolism</topic><topic>Thrombosis - pathology</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mawatari, Kazuaki</creatorcontrib><creatorcontrib>Yoshioka, Emiko</creatorcontrib><creatorcontrib>Toda, Satomi</creatorcontrib><creatorcontrib>Yasui, Sonoko</creatorcontrib><creatorcontrib>Furukawa, Hiroko</creatorcontrib><creatorcontrib>Shimohata, Takaaki</creatorcontrib><creatorcontrib>Ohnishi, Takamasa</creatorcontrib><creatorcontrib>Morishima, Masaki</creatorcontrib><creatorcontrib>Harada, Nagakatsu</creatorcontrib><creatorcontrib>Takahashi, Akira</creatorcontrib><creatorcontrib>Sakaue, Hiroshi</creatorcontrib><creatorcontrib>Nakaya, Yutaka</creatorcontrib><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>Circulation Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mawatari, Kazuaki</au><au>Yoshioka, Emiko</au><au>Toda, Satomi</au><au>Yasui, Sonoko</au><au>Furukawa, Hiroko</au><au>Shimohata, Takaaki</au><au>Ohnishi, Takamasa</au><au>Morishima, Masaki</au><au>Harada, Nagakatsu</au><au>Takahashi, Akira</au><au>Sakaue, Hiroshi</au><au>Nakaya, Yutaka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhancement of Endothelial Function Inhibits Left Atrial Thrombi Development in an Animal Model of Spontaneous Left Atrial Thrombosis</atitle><jtitle>Circulation Journal</jtitle><addtitle>Circ J</addtitle><date>2014</date><risdate>2014</risdate><volume>78</volume><issue>8</issue><spage>1980</spage><epage>1988</epage><pages>1980-1988</pages><issn>1346-9843</issn><eissn>1347-4820</eissn><abstract>Background:Left atrial (LA) thrombosis is an important cause of systemic embolization. The SPORTS rat model of LA thrombi (Spontaneously-Running Tokushima-Shikoku), which have a unique characteristic of high voluntary wheel running, was previously established. The aim of the present study was to investigate how SPORTS rats develop LA thrombi.Methods and Results:Nitric oxide (NO) produced from cardiovascular endothelial cells plays an important protective role in the local regulation of blood flow, vascular tone, and platelet aggregation. No evidence of atrial fibrillation or hypercoagulability in SPORTS rats regardless of age was found; however, SPORTS rats demonstrated endothelial dysfunction and a decrease of NO production from a young age. In addition, endothelial NO synthase activity was significantly decreased in the LA and thoracic aorta endothelia of SPORTS rats. While voluntary wheel running was able to intermittently increase NO levels, running did not statistically decrease the incidence of LA thrombi at autopsy. However, L-arginine treatment significantly increased NO production and provided protection from the development of LA thrombi in SPORTS rats.Conclusions:They present study results indicate that NO has an important role in the development of LA thrombus, and endothelia pathways could provide new targets of therapy to prevent LA thrombosis. (Circ J 2014; 78: 1980–1988)</abstract><cop>Japan</cop><pub>The Japanese Circulation Society</pub><pmid>24859498</pmid><doi>10.1253/circj.CJ-13-1398</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Atrial fibrillation Disease Models, Animal Endothelial dysfunction Endothelium - metabolism Endothelium - pathology Female Heart Atria - metabolism Male Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type III - metabolism Rats Thrombosis Thrombosis - metabolism Thrombosis - pathology Vasodilation |
| title | Enhancement of Endothelial Function Inhibits Left Atrial Thrombi Development in an Animal Model of Spontaneous Left Atrial Thrombosis |
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