Adaptation to hypoxia prevents disturbances in cerebral blood flow during neurodegenerative process.
The rats with neurodegenerative brain disorder induced by administration of a toxic fragment of beta-amyloid demonstrate weakened endothelium-dependent dilation of cerebral vessels, which attested to impaired production of endothelial NO. At the same time, toxic beta-amyloid fragment induced the formation of NO depots in the walls of cerebral vessels, which indirectly attests to NO overproduction in the brain tissue. Preadaptation to hypoxia prevented endothelial dysfunction and improved the efficiency of NO storage. Our results suggest that adaptation to hypoxia protects the brain from various changes in NO production during neurodegenerative damage.
Mashina
S Yu
SY
Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow.
Aleksandrin
V V
VV
Goryacheva
A V
AV
Vlasova
M A
MA
Vanin
A F
AF
Malyshev
I Yu
IY
Manukhina
E B
EB
D000222:Adaptation, Physiological / Q000502:physiology*; D016229:Amyloid beta-Peptides / Q000633:toxicity; D000818:Animals; D001808:Blood Vessels / Q000378:metabolism*; D001921:Brain / Q000098:blood supply*; D004727:Endothelium / Q000187:drug effects / Q000378:metabolism; D000860:Hypoxia / Q000503:physiopathology*; D007501:Iron; D008297:Male; D019636:Neurodegenerative Diseases / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D009569:Nitric Oxide / Q000378:metabolism*; D009589:Nitrogen Oxides; D010446:Peptide Fragments / Q000633:toxicity; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000502:physiology
D016229:Amyloid beta-Peptides; D009589:Nitrogen Oxides; D010446:Peptide Fragments; D009569:Nitric Oxide; C073661:dinitrosyl iron complex; D007501:Iron