scholarly journals Roles of neuronal nitric oxide synthase, oxidative stress, and propofol in N -methyl- d -aspartate-induced dilatation of cerebral arterioles

2012 ◽  
Vol 108 (1) ◽  
pp. 21-29 ◽  
Author(s):  
K. Hama-Tomioka ◽  
H. Kinoshita ◽  
K. Nakahata ◽  
T. Kondo ◽  
T. Azma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Cerebral Arterioles ◽  
Oxide Synthase

scholarly journals Reduced neuronal nitric oxide synthase expression contributes to cardiac oxidative stress and nitroso-redox imbalance in ob/ob mice

Nitric Oxide ◽  
2007 ◽  
Vol 16 (3) ◽  
pp. 331-338 ◽  
Author(s):  
Roberto M. Saraiva ◽  
Khalid M. Minhas ◽  
Meizi Zheng ◽  
Eleanor Pitz ◽  
Adriana Treuer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Redox Imbalance ◽  
Oxide Synthase

scholarly journals Neuronal nitric oxide synthase protects neuroblastoma cells from oxidative stress mediated by garlic derivatives

2007 ◽  
Vol 101 (5) ◽  
pp. 1327-1337 ◽  
Author(s):  
Katia Aquilano ◽  
Giuseppe Filomeni ◽  
Sara Baldelli ◽  
Sara Piccirillo ◽  
Angelo De Martino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuroblastoma Cells ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase

P130. Reduced neuronal nitric oxide synthase expression contributes to increased oxidative stress and nitroso-redox imbalance in murine model of obesity

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 60 ◽  
Author(s):  
Roberto M. Saraiva ◽  
Meizi Zheng ◽  
Khalid M. Minhas ◽  
Eleanor Pitz ◽  
Karl H. Schuleri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Murine Model ◽  
Neuronal Nitric Oxide Synthase ◽  
Redox Imbalance ◽  
Oxide Synthase

scholarly journals Propofol Restores Brain Microvascular Function Impaired by High Glucose via  the Decrease in Oxidative Stress

2008 ◽  
Vol 108 (2) ◽  
pp. 269-275 ◽  
Author(s):  
Katsutoshi Nakahata ◽  
Hiroyuki Kinoshita ◽  
Toshiharu Azma ◽  
Naoyuki Matsuda ◽  
Keiko Hama-Tomioka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
High Glucose ◽  
Brain Slice ◽  
Brain Slices ◽  
Neuronal Nitric Oxide Synthase ◽  
Superoxide Production ◽  
Oxide Synthase ◽  
The Brain

Background Vascular dysfunction induced by hyperglycemia has not been studied in cerebral parenchymal circulation. The current study was designed to examine whether high glucose impairs dilation of cerebral parenchymal arterioles via nitric oxide synthase, and whether propofol recovers this vasodilation by reducing superoxide levels in the brain. Methods Cerebral parenchymal arterioles in the rat brain slices were monitored using computer-assisted videomicroscopy. Vasodilation induced by acetylcholine (10 to 10 m) was obtained after the incubation of brain slices for 60 min with any addition of l-glucose (20 mm), d-glucose (20 mm), or propofol (3 x 10 or 10 m) in combination with d-glucose (20 mm). Superoxide production in the brain slice was determined by dihydroethidium (2 x 10 m) fluorescence. Results Addition of d-glucose, but not l-glucose, reduced arteriolar dilation by acetylcholine, whereas the dilation was abolished by the neuronal nitric oxide synthase inhibitor S-methyl-l-thiocitrulline (10 m). Both propofol and the superoxide dismutase mimetic Tempol (10 m) restored the arteriolar dilation in response to acetylcholine in the brain slice treated with d-glucose. Addition of d-glucose increased superoxide production in the brain slice, whereas propofol, Tempol, and the nicotinamide adenine dinucleotide phosphate (NAD[P]H) oxidase inhibitor apocynin (1 mm) similarly inhibited it. Conclusions Clinically relevant concentrations of propofol ameliorate neuronal nitric oxide synthase-dependent dilation impaired by high glucose in the cerebral parenchymal arterioles via the effect on superoxide levels. Propofol may be protective against cerebral microvascular malfunction resulting from oxidative stress by acute hyperglycemia.

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