Impairment of the Modulatory Role of Nitric Oxide on the Endothelin-1-elicited Contraction of Cerebral Arteries: A Pathogenetic Factor in Cerebral Vasospasm after Subarachnoid Hemorrhage?
Author:
Affiliation:
1. Departamento de Fisiologia, Universidad de Valencia, Valencia, Spain
2. Centro de Investigacion, Hospital Universitario “La Fe”, Valencia, Spain
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Clinical Neurology,Surgery
Link
http://academic.oup.com/neurosurgery/article-pdf/41/1/245/24748270/00006123-199707000-00039.pdf
Reference39 articles.
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2. Enhanced vasoconstrictor effect of endothelin in cerebral arteries from rats with subarachnoid haemorrhage;Alafaci;Acta Physiol Scand,1990
3. Increased endothelial cell turnover in areas of in vivo Evans blue uptake in the pig aorta;Caplan;Atherosclerosis,1973
4. Pressor effects of circulating endothelin are limited by its removal in the pulmonary circulation and by the release of prostacyclin and endothelium-derived relaxing factor;De Nucci;Proc Natl Acad Sci U S A,1988
5. The effect of chronic subarachnoid hemorrhage on basal endothelium-derived relaxing factor activity in intrathecal cerebral arteries;Edwards;J Neurosurg,1992
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