Nitric Oxide Synthase Inhibition in Humans Reduces Cerebral Blood Flow but Not the Hyperemic Response to Hypercapnia | Zendy

Richard P. White | Zendy; Colin Deane | Zendy; Patrick Vallance | Zendy; Hugh S. Markus | Zendy

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Nitric Oxide Synthase Inhibition in Humans Reduces Cerebral Blood Flow but Not the Hyperemic Response to Hypercapnia

Author(s) -

Richard P. White,

Colin Deane,

Patrick Vallance,

Hugh S. Markus

Publication year - 1998

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/01.str.29.2.467

Subject(s) - medicine , hypercapnia , middle cerebral artery , omega n methylarginine , cerebral blood flow , nitric oxide synthase , blood flow , anesthesia , vasodilation , transcranial doppler , hemodynamics , cerebral circulation , nitric oxide , ischemia , acidosis

Animal studies suggest that nitric oxide (NO) is important in basal cerebral blood flow (CBF) regulation and that it may mediate the vasodilatory response to carbon dioxide. We investigated its role in the human circulation using the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA).

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