Role of nitric oxide in the CBF autoregulation during acute stage after subarachnoid haemorrhage in rat pial artery.
The present study was aimed to identify whether endogenously produced nitric oxide (NO) plays a role in preservation of cerebral blood flow (CBF) autoregulation in rat pial artery during the acute stage after subarachnoid haemorrhage (SAH). During the acute stage after SAH, the lower limit of CBF autoregulation significantly shifted to the higher arterial blood pressure in association with suppressed vasodilatation in response to acute hypotension, which was accompanied by significantly increased expression of endothelial nitric oxide synthase mRNA and increased production of superoxide anion in cerebral vessels. SAH-induced increase in superoxide production was further enhanced under pretreatment with N-nitro-L-arginine methyl ester in the cerebral vessels. Following additional administration of L-arginine (100 mg/kg, i.p.), the haemodynamic alterations were significantly restored in association with significantly reduced superoxide level in the cerebral vessels. In line with these findings, rats that received polyethylene glycol superoxide dismutase and catalase or Mn(III) tetrakis (4-benzoic acid) porphyrin chloride showed recovery of impaired autoregulatory vasodilation in response to acute hypotension. Thus, it is suggested that NO endogenously produced is importantly implicated in the preservation of CBF autoregulation during the acute stage after SAH via its capability to scavenge superoxide anion.
Cho
Hyun Gee
HG
Department of Pharmacology, College of Medicine, Pusan National University, Busan, Korea.
Shin
Hwa Kyoung
HK
Shin
Yung Woo
YW
Lee
Jeong Hyun
JH
Hong
Ki Whan
KW
D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008576:Meningeal Arteries / Q000187:drug effects / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000502:physiology; D052250:Nitric Oxide Synthase Type III; D010841:Pia Mater / Q000098:blood supply* / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology / Q000517:prevention & control*
D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D019331:NG-Nitroarginine Methyl Ester