Mechanisms Underlying Potentiation of Endothelin-1-Induced Myofilament Ca2+ Sensitization after Subarachnoid Hemorrhage
نویسندگان
چکیده
منابع مشابه
Mechanisms of vascular dysfunction after subarachnoid hemorrhage.
The main consequence of subarachnoid hemorrhage, for those who survive bleeding, is delayed, persistent vasospasm of intracranial conduit arteries which occurs between the third and seventh day after the insult and results in symptomatic brain ischemia in about 40% of cases. This vasospasm is considered to be a major cause of disability of post-SAH patients. Despite extensive experimental and c...
متن کاملEndothelin B receptor antagonists attenuate subarachnoid hemorrhage-induced cerebral vasospasm.
BACKGROUND AND PURPOSE While it has been widely reported that the vasospasm following subarachnoid hemorrhage (SAH) is prevented/reversed by endothelin (ET) receptor antagonists selective for the ET(A) receptor and by nonselective ET receptor antagonists, ie, antagonists of both the ET(A) and ET(B) receptors, there are no reports on the possible attenuation of the spasm by selective ET(B) recep...
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In the previous issue of Critical Care, Ma and colleagues perform a meta-analysis of five randomized, clinical trials of endothelin antagonists in patients with aneurysmal subarachnoid hemorrhage. There are four trials using clazosentan and one trial with TAK-044. These studies show that endothelin plays an important role in the genesis of angiographic vasospasm. The benefit of these drugs is l...
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Cerebral Vasospasm Induced − Endothelin B Receptor Antagonists Attenuate Subarachnoid Hemorrhage Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1998 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Stroke doi: 10.1161/01.STR.29.9.1924 1998;29:1924-1929 Stroke. http://stroke.ahajournals.org/c...
متن کاملMyofilament Ca2+ sensitization causes susceptibility to cardiac arrhythmia in mice.
In human cardiomyopathy, anatomical abnormalities such as hypertrophy and fibrosis contribute to the risk of ventricular arrhythmias and sudden death. Here we have shown that increased myofilament Ca2+ sensitivity, also a common feature in both inherited and acquired human cardiomyopathies, created arrhythmia susceptibility in mice, even in the absence of anatomical abnormalities. In mice expre...
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ژورنال
عنوان ژورنال: Journal of Cerebral Blood Flow & Metabolism
سال: 2011
ISSN: 0271-678X,1559-7016
DOI: 10.1038/jcbfm.2011.132