Altered NO function contributes to impairment of uPA and tPA cerebrovasodilation after brain injury.
Armstead
William M
WM
Departments of Anesthesia and Pharmacology, University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, USA. armsteaw@uphs.upenn.edu
Cines
Douglas B
DB
Al-Roof Higazi
Abd
A
D000818:Animals; D001930:Brain Injuries / Q000201:enzymology* / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D008297:Male; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology*; D013552:Swine; D010959:Tissue Plasminogen Activator / Q000502:physiology*; D014568:Urokinase-Type Plasminogen Activator / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator