Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hamann, G.
Right arrow Articles by Schimrigk, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hamann, G.
Right arrow Articles by Schimrigk, K.

Stroke, Vol 24, 383-386, Copyright © 1993 by American Heart Association


ARTICLES

Absence of elevation of big endothelin in subarachnoid hemorrhage

G Hamann, E Isenberg, M Strittmatter and K Schimrigk
Department of Neurology, University of the Saarland, Homburg/Saar, FRG.

BACKGROUND AND PURPOSE: Endothelin peptides are potent vasoconstrictors and thus are seen as potential cause of cerebral vasospasm after subarachnoid hemorrhage (SAH). Earlier reports showed elevated or normal endothelin levels in plasma and cerebrospinal fluid in patients suffering from SAH. The present study was designed to determine whether endothelin is a causal factor in SAH. METHODS: We studied 11 patients with acute SAH. Seven of these 11 patients had a proven aneurysm and six had experienced vasospasm. Big endothelin levels were determined by a radioimmunoassay recognizing the C-terminal peptide (normal range, 1- 11 fmol/ml). RESULTS: There were no elevations of big endothelin in the 59 plasma samples and the 17 simultaneously estimated cerebrospinal fluid samples. Differences between plasma and cerebrospinal fluid did not reach significant levels. Big endothelin values between patients with and without vasospasm showed no significant differences. CONCLUSIONS: Our findings suggest that plasma elevation of the endothelins is not reproducible in SAH and that big endothelin is unlikely to be a causal plasma factor in the complex multifactorial development of vasospasm after SAH.


This article has been cited by other articles:


Home page
Exp. Biol. Med.Home page
C.-L. Lin, A. S. Dumont, S.-C. Wu, C.-J. Wang, S.-L. Howng, Y.-F. Huang, W.-Y. Wong, N. F. Kassell, A. Y. Jeng, and A.-L. Kwan
17{beta}-Estradiol Inhibits Endothelin-1 Production and Attenuates Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage.
Experimental Biology and Medicine, June 1, 2006; 231(6): 1054 - 1057.
[Abstract] [Full Text] [PDF]


Home page
StrokeHome page
L. Mascia, L. Fedorko, D. J. Stewart, F. Mohamed, K. terBrugge, V. M. Ranieri, M. C. Wallace, and R. M. Pluta
Temporal Relationship Between Endothelin-1 Concentrations and Cerebral Vasospasm in Patients With Aneurysmal Subarachnoid Hemorrhage Editorial Comment : Endothelin-1 in Vasospasm After SAH
Stroke, May 1, 2001; 32(5): 1185 - 1190.
[Abstract] [Full Text] [PDF]