Literature DB >> 25214428

RAAS and stress markers in acute ischemic stroke: preliminary findings.

C Back1, K L Thiesen, K Skovgaard, L Edvinsson, L T Jensen, V A Larsen, H K Iversen.   

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.
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Entities:  

Keywords:  ischemic stroke; renin angiotensin aldosterone system; stress hormones

Mesh:

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Year:  2014        PMID: 25214428     DOI: 10.1111/ane.12298

Source DB:  PubMed          Journal:  Acta Neurol Scand        ISSN: 0001-6314            Impact factor:   3.209


  4 in total

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