Expression of nitric oxide synthase in the cerebral microvasculature after traumatic brain injury in the rat.
Reduced nicotinamide adenine dinucleotide phosphate-diaphorase (NADPHd) histochemistry and nitric oxide synthase (NOS) immunocytochemistry were performed on sections of brain after moderate traumatic brain injury. There was a pronounced increase in NADPHd reactivity and an induction of the endothelial NOS (eNOS) isoform in microvessels surrounding the cortical contusion by 24 h post-injury. This altered microvascular state may contribute to barrier breakdown and hyperemia which characterize traumatic brain injury.
Cobbs
C S
CS
Department of Neurosurgery, University of California and San Francisco General Hospital, 94110, USA.
Fenoy
A
A
Bredt
D S
DS
Noble
L J
LJ
D000818:Animals; D001808:Blood Vessels / Q000201:enzymology; D001924:Brain Concussion / Q000201:enzymology*; D002560:Cerebrovascular Circulation; D004730:Endothelium, Vascular / Q000201:enzymology; D006651:Histocytochemistry; D007150:Immunohistochemistry; D008833:Microcirculation; D009252:NADPH Dehydrogenase / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D051381:Rats
D019001:Nitric Oxide Synthase; D009252:NADPH Dehydrogenase