Increased intracerebral excitatory amino acids and nitric oxide after hypothermic circulatory arrest

1999 ◽  
Vol 67 (2) ◽  
pp. 371-376 ◽  
Author(s):  
Elaine E Tseng ◽  
Malcolm V Brock ◽  
Christopher C Kwon ◽  
Madhu Annanata ◽  
Mary S Lange ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Amino Acids ◽  
Excitatory Amino Acids ◽  
Circulatory Arrest ◽  
Hypothermic Circulatory Arrest

Neuronal Nitric Oxide Synthase Inhibition Reduces Neuronal Apoptosis After Hypothermic Circulatory Arrest

1997 ◽  
Vol 64 (6) ◽  
pp. 1639-1647 ◽  
Author(s):  
Elaine E Tseng ◽  
Malcolm V Brock ◽  
Mary S Lange ◽  
Mary E Blue ◽  
Juan C Troncoso ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Apoptosis ◽  
Circulatory Arrest ◽  
Neuronal Nitric Oxide Synthase ◽  
Hypothermic Circulatory Arrest ◽  
Oxide Synthase

Nitric oxide production affects cerebral perfusion and metabolism after deep hypothermic circulatory arrest

1996 ◽  
Vol 61 (6) ◽  
pp. 1699-1707 ◽  
Author(s):  
Steven S.L. Tsui ◽  
Paul M. Kirshbom ◽  
Michael J. Davies ◽  
Michael T. Jacobs ◽  
William J. Greeley ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebral Perfusion ◽  
Circulatory Arrest ◽  
Deep Hypothermic Circulatory Arrest ◽  
Hypothermic Circulatory Arrest ◽  
Nitric Oxide Production ◽  
Oxide Production

Nitric oxide contributes to dilatation of cerebral arterioles during seizures

1993 ◽  
Vol 265 (6) ◽  
pp. H2209-H2212 ◽  
Author(s):  
F. M. Faraci ◽  
K. R. Breese ◽  
D. D. Heistad
Keyword(s):  
Nitric Oxide ◽  
Amino Acids ◽  
Arterial Pressure ◽  
Excitatory Amino Acids ◽  
No Synthase ◽  
Cerebral Microcirculation ◽  
Cranial Window ◽  
Cerebral Arterioles ◽  
Endogenous Release ◽  
Arteriolar Diameter

Endogenous release of excitatory amino acids during seizures produces marked increases in neuronal activity and guanosine 3',5'-cyclic monophosphate levels in brain tissue, which are mediated by nitric oxide (NO). We tested the hypothesis that dilatation of the cerebral microcirculation during seizures is mediated by NO. Diameters of cerebral arterioles were measured using a closed cranial window in anesthetized rabbits. Three, five, nine, and eleven minutes after the onset of pentylenetetrazole-induced seizure (which releases endogenous excitatory amino acids), arteriolar diameter increased by 42 +/- 6, 30 +/- 3, 20 +/- 2, and 16 +/- 2% (means +/- SE), respectively, from a control diameter of 86 +/- 6 microns. Arterial pressure was maintained at control levels during seizures. In the presence of NG-nitro-L-arginine (L-NNA, 300 microM), an inhibitor of NO synthase, vasodilatation during seizures was not affected at 3 min (40 +/- 8%) but was significantly reduced at 5, 9, and 11 min (17 +/- 5, 6 +/- 3, and 1 +/- 3%, respectively, P < 0.05 vs. control). Vasodilatation in response to topical application of acetylcholine (1 microM) was also inhibited by L-NNA (33 +/- 5 vs. 3 +/- 2%, P < 0.05). Dilatation of cerebral arterioles in response to nitroprusside (1 and 10 microM) was not inhibited by L-NNA. Thus sustained, but not initial, dilatation of cerebral arterioles during seizures appears to be mediated in part by NO.

Nitric oxide mediates neurologic injury after hypothermic circulatory arrest

1999 ◽  
Vol 67 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Elaine E Tseng ◽  
Malcolm V Brock ◽  
Mary S Lange ◽  
Juan C Troncoso ◽  
Charles J Lowenstein ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Circulatory Arrest ◽  
Hypothermic Circulatory Arrest ◽  
Neurologic Injury
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