RAAS and stress markers in acute ischemic stroke: preliminary findings
Objectives Angiotensin II type 1 receptor blockade has neuroprotective effects in animal stroke models, but no effects in clinical stroke trials. We evaluated cerebral and peripheral changes in the renin angiotensin aldosterone system (RAAS) and stress responses in acute ischemic stroke patients. Ma...
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| Veröffentlicht in: | Acta neurologica Scandinavica 2015-02, Vol.131 (2), p.132-139 |
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| container_title | Acta neurologica Scandinavica |
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| creator | Back, C. Thiesen, K. L. Skovgaard, K. Edvinsson, L. Jensen, L. T. Larsen, V. A. Iversen, H. K. |
| description | Objectives
Angiotensin II type 1 receptor blockade has neuroprotective effects in animal stroke models, but no effects in clinical stroke trials. We evaluated cerebral and peripheral changes in the renin angiotensin aldosterone system (RAAS) and stress responses in acute ischemic stroke patients.
Materials and methods
Blood from a jugular and cubital vein was collected within 48 h of stroke onset, after 24 and 48 h, and renin, angiotensin I, angiotensin II, aldosterone, norepinephrine, epinephrine, and cortisol were measured. Post‐stroke cubital vein samples were collected after 8 (4.7–10) months.
Results
The acute systolic blood pressure was significantly increased, 148 (141–168) vs 140 (130–147) mmHg post‐stroke. Angiotensin I, renin and aldosterone levels were significantly lower, angiotensin II was unchanged, and ACE activity was higher in the acute phase compared to post‐stroke. No differences in RAAS were detected between jugular and cubital plasma levels. Jugular venous plasma levels of epinephrine and cortisol were elevated in the acute phase compared to cubital levels (P |
| doi_str_mv | 10.1111/ane.12298 |
| format | Article |
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Angiotensin II type 1 receptor blockade has neuroprotective effects in animal stroke models, but no effects in clinical stroke trials. We evaluated cerebral and peripheral changes in the renin angiotensin aldosterone system (RAAS) and stress responses in acute ischemic stroke patients.
Materials and methods
Blood from a jugular and cubital vein was collected within 48 h of stroke onset, after 24 and 48 h, and renin, angiotensin I, angiotensin II, aldosterone, norepinephrine, epinephrine, and cortisol were measured. Post‐stroke cubital vein samples were collected after 8 (4.7–10) months.
Results
The acute systolic blood pressure was significantly increased, 148 (141–168) vs 140 (130–147) mmHg post‐stroke. Angiotensin I, renin and aldosterone levels were significantly lower, angiotensin II was unchanged, and ACE activity was higher in the acute phase compared to post‐stroke. No differences in RAAS were detected between jugular and cubital plasma levels. Jugular venous plasma levels of epinephrine and cortisol were elevated in the acute phase compared to cubital levels (P < 0.05).
Conclusion
Increased epinephrine and cortisol levels in the jugular vein blood may reflect a higher peripheral turnover. The observed changes in RAAS in the acute stroke phase are consistent with responses to increased blood pressure.</description><identifier>ISSN: 0001-6314</identifier><identifier>EISSN: 1600-0404</identifier><identifier>DOI: 10.1111/ane.12298</identifier><identifier>PMID: 25214428</identifier><identifier>CODEN: ANRSAS</identifier><language>eng</language><publisher>Denmark: Blackwell Publishing Ltd</publisher><subject>Aged ; Aged, 80 and over ; Aldosterone - blood ; Angiotensin II - blood ; Animals ; Biomarkers - blood ; Blood Pressure ; Female ; Humans ; Hypertension ; ischemic stroke ; Male ; Middle Aged ; Renin - blood ; renin angiotensin aldosterone system ; Renin-Angiotensin System - physiology ; stress hormones ; Stroke - blood ; Stroke - physiopathology</subject><ispartof>Acta neurologica Scandinavica, 2015-02, Vol.131 (2), p.132-139</ispartof><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><rights>Copyright © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4598-7f94a7bf0d6ed4ceb2480c8b995200a9e03c236163d5899fcd91837c8fe2ba963</citedby><cites>FETCH-LOGICAL-c4598-7f94a7bf0d6ed4ceb2480c8b995200a9e03c236163d5899fcd91837c8fe2ba963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fane.12298$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fane.12298$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25214428$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Back, C.</creatorcontrib><creatorcontrib>Thiesen, K. L.</creatorcontrib><creatorcontrib>Skovgaard, K.</creatorcontrib><creatorcontrib>Edvinsson, L.</creatorcontrib><creatorcontrib>Jensen, L. T.</creatorcontrib><creatorcontrib>Larsen, V. A.</creatorcontrib><creatorcontrib>Iversen, H. K.</creatorcontrib><title>RAAS and stress markers in acute ischemic stroke: preliminary findings</title><title>Acta neurologica Scandinavica</title><addtitle>Acta Neurol Scand</addtitle><description>Objectives
Angiotensin II type 1 receptor blockade has neuroprotective effects in animal stroke models, but no effects in clinical stroke trials. We evaluated cerebral and peripheral changes in the renin angiotensin aldosterone system (RAAS) and stress responses in acute ischemic stroke patients.
Materials and methods
Blood from a jugular and cubital vein was collected within 48 h of stroke onset, after 24 and 48 h, and renin, angiotensin I, angiotensin II, aldosterone, norepinephrine, epinephrine, and cortisol were measured. Post‐stroke cubital vein samples were collected after 8 (4.7–10) months.
Results
The acute systolic blood pressure was significantly increased, 148 (141–168) vs 140 (130–147) mmHg post‐stroke. Angiotensin I, renin and aldosterone levels were significantly lower, angiotensin II was unchanged, and ACE activity was higher in the acute phase compared to post‐stroke. No differences in RAAS were detected between jugular and cubital plasma levels. Jugular venous plasma levels of epinephrine and cortisol were elevated in the acute phase compared to cubital levels (P < 0.05).
Conclusion
Increased epinephrine and cortisol levels in the jugular vein blood may reflect a higher peripheral turnover. The observed changes in RAAS in the acute stroke phase are consistent with responses to increased blood pressure.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aldosterone - blood</subject><subject>Angiotensin II - blood</subject><subject>Animals</subject><subject>Biomarkers - blood</subject><subject>Blood Pressure</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertension</subject><subject>ischemic stroke</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Renin - blood</subject><subject>renin angiotensin aldosterone system</subject><subject>Renin-Angiotensin System - physiology</subject><subject>stress hormones</subject><subject>Stroke - blood</subject><subject>Stroke - physiopathology</subject><issn>0001-6314</issn><issn>1600-0404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUtP3DAURq2qqAy0C_4AitRNWQSuHdux2Y14i6egVZeW49wUQx5TeyKYf49hgEUlpHpjWTr3yPf7CNmgsE3T2bE9blPGtPpEJlQC5MCBfyYTAKC5LChfJWsx3qUXKzn_QlaZYJRzpibk8Ho6vclsX2dxHjDGrLPhHkPMfJ9ZN84x89HdYufdMzDc4242C9j6zvc2LLLG97Xv_8SvZKWxbcRvr_c6-XV48HPvOD-7PDrZm57ljgut8rLR3JZVA7XEmjusGFfgVKW1YABWIxSOFZLKohZK68bVmqqidKpBVlkti3XyY-mdheHviHFuuvQ_bNsUwTBGQ6UEzoRS-j9QwTiUKZ2Efv8HvRvG0KdFEsUVAw2UJmprSbkwxBiwMbPgU1wLQ8E892CS2bz0kNjNV-NYdVi_k2_BJ2BnCTz4Fhcfm8z04uBNmS8nfJzj4_tEqsvIsiiF-X1xZM7FqbjaPxcGiid4354N</recordid><startdate>201502</startdate><enddate>201502</enddate><creator>Back, C.</creator><creator>Thiesen, K. L.</creator><creator>Skovgaard, K.</creator><creator>Edvinsson, L.</creator><creator>Jensen, L. T.</creator><creator>Larsen, V. A.</creator><creator>Iversen, H. K.</creator><general>Blackwell Publishing Ltd</general><general>Hindawi Limited</general><scope>BSCLL</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>7TK</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201502</creationdate><title>RAAS and stress markers in acute ischemic stroke: preliminary findings</title><author>Back, C. ; Thiesen, K. L. ; Skovgaard, K. ; Edvinsson, L. ; Jensen, L. T. ; Larsen, V. A. ; Iversen, H. K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4598-7f94a7bf0d6ed4ceb2480c8b995200a9e03c236163d5899fcd91837c8fe2ba963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aldosterone - blood</topic><topic>Angiotensin II - blood</topic><topic>Animals</topic><topic>Biomarkers - blood</topic><topic>Blood Pressure</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertension</topic><topic>ischemic stroke</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Renin - blood</topic><topic>renin angiotensin aldosterone system</topic><topic>Renin-Angiotensin System - physiology</topic><topic>stress hormones</topic><topic>Stroke - blood</topic><topic>Stroke - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Back, C.</creatorcontrib><creatorcontrib>Thiesen, K. L.</creatorcontrib><creatorcontrib>Skovgaard, K.</creatorcontrib><creatorcontrib>Edvinsson, L.</creatorcontrib><creatorcontrib>Jensen, L. T.</creatorcontrib><creatorcontrib>Larsen, V. A.</creatorcontrib><creatorcontrib>Iversen, H. K.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Acta neurologica Scandinavica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Back, C.</au><au>Thiesen, K. L.</au><au>Skovgaard, K.</au><au>Edvinsson, L.</au><au>Jensen, L. T.</au><au>Larsen, V. A.</au><au>Iversen, H. K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RAAS and stress markers in acute ischemic stroke: preliminary findings</atitle><jtitle>Acta neurologica Scandinavica</jtitle><addtitle>Acta Neurol Scand</addtitle><date>2015-02</date><risdate>2015</risdate><volume>131</volume><issue>2</issue><spage>132</spage><epage>139</epage><pages>132-139</pages><issn>0001-6314</issn><eissn>1600-0404</eissn><coden>ANRSAS</coden><abstract>Objectives
Angiotensin II type 1 receptor blockade has neuroprotective effects in animal stroke models, but no effects in clinical stroke trials. We evaluated cerebral and peripheral changes in the renin angiotensin aldosterone system (RAAS) and stress responses in acute ischemic stroke patients.
Materials and methods
Blood from a jugular and cubital vein was collected within 48 h of stroke onset, after 24 and 48 h, and renin, angiotensin I, angiotensin II, aldosterone, norepinephrine, epinephrine, and cortisol were measured. Post‐stroke cubital vein samples were collected after 8 (4.7–10) months.
Results
The acute systolic blood pressure was significantly increased, 148 (141–168) vs 140 (130–147) mmHg post‐stroke. Angiotensin I, renin and aldosterone levels were significantly lower, angiotensin II was unchanged, and ACE activity was higher in the acute phase compared to post‐stroke. No differences in RAAS were detected between jugular and cubital plasma levels. Jugular venous plasma levels of epinephrine and cortisol were elevated in the acute phase compared to cubital levels (P < 0.05).
Conclusion
Increased epinephrine and cortisol levels in the jugular vein blood may reflect a higher peripheral turnover. The observed changes in RAAS in the acute stroke phase are consistent with responses to increased blood pressure.</abstract><cop>Denmark</cop><pub>Blackwell Publishing Ltd</pub><pmid>25214428</pmid><doi>10.1111/ane.12298</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Aged, 80 and over Aldosterone - blood Angiotensin II - blood Animals Biomarkers - blood Blood Pressure Female Humans Hypertension ischemic stroke Male Middle Aged Renin - blood renin angiotensin aldosterone system Renin-Angiotensin System - physiology stress hormones Stroke - blood Stroke - physiopathology |
| title | RAAS and stress markers in acute ischemic stroke: preliminary findings |
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