Molecular Profile of Vascular Ion Channels After Experimental Subarachnoid Hemorrhage
Cerebral vasospasm is a transient, delayed constriction of cerebral arteries that occurs after subarachnoid hemorrhage (SAH). Smooth muscle cells show impaired relaxation after SAH, which may be caused by a defect in the ionic mechanisms regulating smooth muscle membrane potential and Ca2+ permeabil...
Gespeichert in:
| Veröffentlicht in: | Journal of cerebral blood flow and metabolism 2004-01, Vol.24 (1), p.75-83 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 83 |
|---|---|
| container_issue | 1 |
| container_start_page | 75 |
| container_title | Journal of cerebral blood flow and metabolism |
| container_volume | 24 |
| creator | Aihara, Yasuo Jahromi, Babak S. Yassari, Reza Nikitina, Elena Agbaje-Williams, Mayowa Macdonald, R. Loch |
| description | Cerebral vasospasm is a transient, delayed constriction of cerebral arteries that occurs after subarachnoid hemorrhage (SAH). Smooth muscle cells show impaired relaxation after SAH, which may be caused by a defect in the ionic mechanisms regulating smooth muscle membrane potential and Ca2+ permeability. We tested this hypothesis by examining changes in expression of mRNA and protein for ion channels in the basilar arteries of dogs after SAH using quantitative real-time polymerase chain reaction (PCR) and western blotting. SAH was associated with a significant reduction in basilar artery diameter to 41 ± 8% of pre-SAH diameter (P < 0.001) after 7 days. There was significant downregulation of the voltage-gated K+ channel Kv 2.2 (65% reduction in mRNA, P < 0.001; 49% reduction in protein, P < 0.05) and the β1 subunit of the large-conductance, Ca2+-activated K+ (BK) channel (53% reduction in mRNA, P < 0.02). There was no change in BK β1 subunit protein. Changes in mRNA levels of Kv 2.2 and the BK-β1 subunit correlated with the degree of vasospasm (r2 = 0.490 and 0.529 respectively, P < 0.05). The inwardly rectifying K+ (Kir) channel Kir 2.1 was upregulated (234% increase in mRNA, P < 0.001; 350% increase in protein, P < 0.001). There was no significant change in mRNA expression of L- type Ca2+ channels and the BK-α subunit. These data suggest that K+ channel dysfunction may contribute to the pathogenesis of cerebral vasospasm. |
| doi_str_mv | 10.1097/01.WCB.0000095803.98378.D8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_80067071</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1097_01.WCB.0000095803.98378.D8</sage_id><sourcerecordid>80067071</sourcerecordid><originalsourceid>FETCH-LOGICAL-c560t-2245e38a9e021335faf150511a27b444ea1906aceaf4069fe9909840b32f44323</originalsourceid><addsrcrecordid>eNqNkE1v1DAQhi0EokvhJ4CiSnBLGMfxF7eyLbRSEUhQ4GbNpmM2VTbe2onU_nu8ZMVKnPDFkvW843cexk44VBysfgu8-rF8X8HuWGlAVNYIbaoz84gtuJS21MDVY7aAWvNSafPziD1L6TbjRkj5lB3xRhmjuF2w60-hp3bqMRZfYvBdT0XwxXdM89tlGIrlGoeB-lSc-pFicX6_pdhtaBixL75OK4zYrofQ3RQXtAkxrvEXPWdPPPaJXuzvY3b94fzb8qK8-vzxcnl6VbZSwVjWdSNJGLQENRdCevRcguQca71qmoaQW1DYEvoGlPVkLVjTwErUvmlELY7Zm3nuNoa7idLoNl1qqe9xoDAlZwCUBs0zePIPeBumOORuruZWCqvlbtq7GWpjSCmSd9u8KMYHx8HtzDvgLpt3B_Puj3l3ZnL41f6HabWhm0N0rzoDr_dAlou9jzi0XTpwUqoalMycnrmURR5q_leFl3NywHGK9He0lTZrNeI3UPKkzw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>219539752</pqid></control><display><type>article</type><title>Molecular Profile of Vascular Ion Channels After Experimental Subarachnoid Hemorrhage</title><source>Access via SAGE</source><source>MEDLINE</source><creator>Aihara, Yasuo ; Jahromi, Babak S. ; Yassari, Reza ; Nikitina, Elena ; Agbaje-Williams, Mayowa ; Macdonald, R. Loch</creator><creatorcontrib>Aihara, Yasuo ; Jahromi, Babak S. ; Yassari, Reza ; Nikitina, Elena ; Agbaje-Williams, Mayowa ; Macdonald, R. Loch</creatorcontrib><description><![CDATA[Cerebral vasospasm is a transient, delayed constriction of cerebral arteries that occurs after subarachnoid hemorrhage (SAH). Smooth muscle cells show impaired relaxation after SAH, which may be caused by a defect in the ionic mechanisms regulating smooth muscle membrane potential and Ca2+ permeability. We tested this hypothesis by examining changes in expression of mRNA and protein for ion channels in the basilar arteries of dogs after SAH using quantitative real-time polymerase chain reaction (PCR) and western blotting. SAH was associated with a significant reduction in basilar artery diameter to 41 ± 8% of pre-SAH diameter (P < 0.001) after 7 days. There was significant downregulation of the voltage-gated K+ channel Kv 2.2 (65% reduction in mRNA, P < 0.001; 49% reduction in protein, P < 0.05) and the β1 subunit of the large-conductance, Ca2+-activated K+ (BK) channel (53% reduction in mRNA, P < 0.02). There was no change in BK β1 subunit protein. Changes in mRNA levels of Kv 2.2 and the BK-β1 subunit correlated with the degree of vasospasm (r2 = 0.490 and 0.529 respectively, P < 0.05). The inwardly rectifying K+ (Kir) channel Kir 2.1 was upregulated (234% increase in mRNA, P < 0.001; 350% increase in protein, P < 0.001). There was no significant change in mRNA expression of L- type Ca2+ channels and the BK-α subunit. These data suggest that K+ channel dysfunction may contribute to the pathogenesis of cerebral vasospasm.]]></description><identifier>ISSN: 0271-678X</identifier><identifier>EISSN: 1559-7016</identifier><identifier>DOI: 10.1097/01.WCB.0000095803.98378.D8</identifier><identifier>PMID: 14688619</identifier><identifier>CODEN: JCBMDN</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Animals ; Basilar Artery - anatomy & histology ; Basilar Artery - physiology ; Biological and medical sciences ; Blood Vessels - metabolism ; Blotting, Western ; Calcium Channels, L-Type - biosynthesis ; Calcium Channels, L-Type - genetics ; Coronary Vasospasm - metabolism ; Delayed Rectifier Potassium Channels ; Dogs ; Gene Targeting ; Ion Channels - metabolism ; Large-Conductance Calcium-Activated Potassium Channels ; Medical sciences ; Neurology ; Potassium Channels - metabolism ; Potassium Channels, Calcium-Activated - metabolism ; Potassium Channels, Inwardly Rectifying ; Potassium Channels, Voltage-Gated ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - biosynthesis ; Subarachnoid Hemorrhage - metabolism ; Up-Regulation - physiology ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of cerebral blood flow and metabolism, 2004-01, Vol.24 (1), p.75-83</ispartof><rights>2003 The International Society for Cerebral Blood Flow and Metabolism</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-2245e38a9e021335faf150511a27b444ea1906aceaf4069fe9909840b32f44323</citedby><cites>FETCH-LOGICAL-c560t-2245e38a9e021335faf150511a27b444ea1906aceaf4069fe9909840b32f44323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1097/01.WCB.0000095803.98378.D8$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1097/01.WCB.0000095803.98378.D8$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,4024,21819,27923,27924,27925,43621,43622</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15562065$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14688619$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aihara, Yasuo</creatorcontrib><creatorcontrib>Jahromi, Babak S.</creatorcontrib><creatorcontrib>Yassari, Reza</creatorcontrib><creatorcontrib>Nikitina, Elena</creatorcontrib><creatorcontrib>Agbaje-Williams, Mayowa</creatorcontrib><creatorcontrib>Macdonald, R. Loch</creatorcontrib><title>Molecular Profile of Vascular Ion Channels After Experimental Subarachnoid Hemorrhage</title><title>Journal of cerebral blood flow and metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description><![CDATA[Cerebral vasospasm is a transient, delayed constriction of cerebral arteries that occurs after subarachnoid hemorrhage (SAH). Smooth muscle cells show impaired relaxation after SAH, which may be caused by a defect in the ionic mechanisms regulating smooth muscle membrane potential and Ca2+ permeability. We tested this hypothesis by examining changes in expression of mRNA and protein for ion channels in the basilar arteries of dogs after SAH using quantitative real-time polymerase chain reaction (PCR) and western blotting. SAH was associated with a significant reduction in basilar artery diameter to 41 ± 8% of pre-SAH diameter (P < 0.001) after 7 days. There was significant downregulation of the voltage-gated K+ channel Kv 2.2 (65% reduction in mRNA, P < 0.001; 49% reduction in protein, P < 0.05) and the β1 subunit of the large-conductance, Ca2+-activated K+ (BK) channel (53% reduction in mRNA, P < 0.02). There was no change in BK β1 subunit protein. Changes in mRNA levels of Kv 2.2 and the BK-β1 subunit correlated with the degree of vasospasm (r2 = 0.490 and 0.529 respectively, P < 0.05). The inwardly rectifying K+ (Kir) channel Kir 2.1 was upregulated (234% increase in mRNA, P < 0.001; 350% increase in protein, P < 0.001). There was no significant change in mRNA expression of L- type Ca2+ channels and the BK-α subunit. These data suggest that K+ channel dysfunction may contribute to the pathogenesis of cerebral vasospasm.]]></description><subject>Animals</subject><subject>Basilar Artery - anatomy & histology</subject><subject>Basilar Artery - physiology</subject><subject>Biological and medical sciences</subject><subject>Blood Vessels - metabolism</subject><subject>Blotting, Western</subject><subject>Calcium Channels, L-Type - biosynthesis</subject><subject>Calcium Channels, L-Type - genetics</subject><subject>Coronary Vasospasm - metabolism</subject><subject>Delayed Rectifier Potassium Channels</subject><subject>Dogs</subject><subject>Gene Targeting</subject><subject>Ion Channels - metabolism</subject><subject>Large-Conductance Calcium-Activated Potassium Channels</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Potassium Channels - metabolism</subject><subject>Potassium Channels, Calcium-Activated - metabolism</subject><subject>Potassium Channels, Inwardly Rectifying</subject><subject>Potassium Channels, Voltage-Gated</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Subarachnoid Hemorrhage - metabolism</subject><subject>Up-Regulation - physiology</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0271-678X</issn><issn>1559-7016</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkE1v1DAQhi0EokvhJ4CiSnBLGMfxF7eyLbRSEUhQ4GbNpmM2VTbe2onU_nu8ZMVKnPDFkvW843cexk44VBysfgu8-rF8X8HuWGlAVNYIbaoz84gtuJS21MDVY7aAWvNSafPziD1L6TbjRkj5lB3xRhmjuF2w60-hp3bqMRZfYvBdT0XwxXdM89tlGIrlGoeB-lSc-pFicX6_pdhtaBixL75OK4zYrofQ3RQXtAkxrvEXPWdPPPaJXuzvY3b94fzb8qK8-vzxcnl6VbZSwVjWdSNJGLQENRdCevRcguQca71qmoaQW1DYEvoGlPVkLVjTwErUvmlELY7Zm3nuNoa7idLoNl1qqe9xoDAlZwCUBs0zePIPeBumOORuruZWCqvlbtq7GWpjSCmSd9u8KMYHx8HtzDvgLpt3B_Puj3l3ZnL41f6HabWhm0N0rzoDr_dAlou9jzi0XTpwUqoalMycnrmURR5q_leFl3NywHGK9He0lTZrNeI3UPKkzw</recordid><startdate>200401</startdate><enddate>200401</enddate><creator>Aihara, Yasuo</creator><creator>Jahromi, Babak S.</creator><creator>Yassari, Reza</creator><creator>Nikitina, Elena</creator><creator>Agbaje-Williams, Mayowa</creator><creator>Macdonald, R. Loch</creator><general>SAGE Publications</general><general>Lippincott Williams & Wilkins</general><general>Sage Publications Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200401</creationdate><title>Molecular Profile of Vascular Ion Channels After Experimental Subarachnoid Hemorrhage</title><author>Aihara, Yasuo ; Jahromi, Babak S. ; Yassari, Reza ; Nikitina, Elena ; Agbaje-Williams, Mayowa ; Macdonald, R. Loch</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-2245e38a9e021335faf150511a27b444ea1906aceaf4069fe9909840b32f44323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Basilar Artery - anatomy & histology</topic><topic>Basilar Artery - physiology</topic><topic>Biological and medical sciences</topic><topic>Blood Vessels - metabolism</topic><topic>Blotting, Western</topic><topic>Calcium Channels, L-Type - biosynthesis</topic><topic>Calcium Channels, L-Type - genetics</topic><topic>Coronary Vasospasm - metabolism</topic><topic>Delayed Rectifier Potassium Channels</topic><topic>Dogs</topic><topic>Gene Targeting</topic><topic>Ion Channels - metabolism</topic><topic>Large-Conductance Calcium-Activated Potassium Channels</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Potassium Channels - metabolism</topic><topic>Potassium Channels, Calcium-Activated - metabolism</topic><topic>Potassium Channels, Inwardly Rectifying</topic><topic>Potassium Channels, Voltage-Gated</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Subarachnoid Hemorrhage - metabolism</topic><topic>Up-Regulation - physiology</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aihara, Yasuo</creatorcontrib><creatorcontrib>Jahromi, Babak S.</creatorcontrib><creatorcontrib>Yassari, Reza</creatorcontrib><creatorcontrib>Nikitina, Elena</creatorcontrib><creatorcontrib>Agbaje-Williams, Mayowa</creatorcontrib><creatorcontrib>Macdonald, R. Loch</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cerebral blood flow and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aihara, Yasuo</au><au>Jahromi, Babak S.</au><au>Yassari, Reza</au><au>Nikitina, Elena</au><au>Agbaje-Williams, Mayowa</au><au>Macdonald, R. Loch</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular Profile of Vascular Ion Channels After Experimental Subarachnoid Hemorrhage</atitle><jtitle>Journal of cerebral blood flow and metabolism</jtitle><addtitle>J Cereb Blood Flow Metab</addtitle><date>2004-01</date><risdate>2004</risdate><volume>24</volume><issue>1</issue><spage>75</spage><epage>83</epage><pages>75-83</pages><issn>0271-678X</issn><eissn>1559-7016</eissn><coden>JCBMDN</coden><abstract><![CDATA[Cerebral vasospasm is a transient, delayed constriction of cerebral arteries that occurs after subarachnoid hemorrhage (SAH). Smooth muscle cells show impaired relaxation after SAH, which may be caused by a defect in the ionic mechanisms regulating smooth muscle membrane potential and Ca2+ permeability. We tested this hypothesis by examining changes in expression of mRNA and protein for ion channels in the basilar arteries of dogs after SAH using quantitative real-time polymerase chain reaction (PCR) and western blotting. SAH was associated with a significant reduction in basilar artery diameter to 41 ± 8% of pre-SAH diameter (P < 0.001) after 7 days. There was significant downregulation of the voltage-gated K+ channel Kv 2.2 (65% reduction in mRNA, P < 0.001; 49% reduction in protein, P < 0.05) and the β1 subunit of the large-conductance, Ca2+-activated K+ (BK) channel (53% reduction in mRNA, P < 0.02). There was no change in BK β1 subunit protein. Changes in mRNA levels of Kv 2.2 and the BK-β1 subunit correlated with the degree of vasospasm (r2 = 0.490 and 0.529 respectively, P < 0.05). The inwardly rectifying K+ (Kir) channel Kir 2.1 was upregulated (234% increase in mRNA, P < 0.001; 350% increase in protein, P < 0.001). There was no significant change in mRNA expression of L- type Ca2+ channels and the BK-α subunit. These data suggest that K+ channel dysfunction may contribute to the pathogenesis of cerebral vasospasm.]]></abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>14688619</pmid><doi>10.1097/01.WCB.0000095803.98378.D8</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0271-678X |
| ispartof | Journal of cerebral blood flow and metabolism, 2004-01, Vol.24 (1), p.75-83 |
| issn | 0271-678X 1559-7016 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_80067071 |
| source | Access via SAGE; MEDLINE |
| subjects | Animals Basilar Artery - anatomy & histology Basilar Artery - physiology Biological and medical sciences Blood Vessels - metabolism Blotting, Western Calcium Channels, L-Type - biosynthesis Calcium Channels, L-Type - genetics Coronary Vasospasm - metabolism Delayed Rectifier Potassium Channels Dogs Gene Targeting Ion Channels - metabolism Large-Conductance Calcium-Activated Potassium Channels Medical sciences Neurology Potassium Channels - metabolism Potassium Channels, Calcium-Activated - metabolism Potassium Channels, Inwardly Rectifying Potassium Channels, Voltage-Gated Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - biosynthesis Subarachnoid Hemorrhage - metabolism Up-Regulation - physiology Vascular diseases and vascular malformations of the nervous system |
| title | Molecular Profile of Vascular Ion Channels After Experimental Subarachnoid Hemorrhage |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-20T11%3A41%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Molecular%20Profile%20of%20Vascular%20Ion%20Channels%20After%20Experimental%20Subarachnoid%20Hemorrhage&rft.jtitle=Journal%20of%20cerebral%20blood%20flow%20and%20metabolism&rft.au=Aihara,%20Yasuo&rft.date=2004-01&rft.volume=24&rft.issue=1&rft.spage=75&rft.epage=83&rft.pages=75-83&rft.issn=0271-678X&rft.eissn=1559-7016&rft.coden=JCBMDN&rft_id=info:doi/10.1097/01.WCB.0000095803.98378.D8&rft_dat=%3Cproquest_cross%3E80067071%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=219539752&rft_id=info:pmid/14688619&rft_sage_id=10.1097_01.WCB.0000095803.98378.D8&rfr_iscdi=true |