Distribution of inducible nitric oxide synthase and cell proliferation in rat brain after transient middle cerebral artery occlusion

2006 ◽  
Vol 1093 (1) ◽  
pp. 190-197 ◽  
Author(s):  
Yoshihide Sehara ◽  
Takeshi Hayashi ◽  
Kentaro Deguchi ◽  
Shoko Nagotani ◽  
Hanzhe Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Nitric Oxide Synthase ◽  
Middle Cerebral Artery ◽  
Rat Brain ◽  
Inducible Nitric Oxide Synthase ◽  
Artery Occlusion ◽  
Oxide Synthase ◽  
Cerebral Artery Occlusion ◽  
Inducible Nitric Oxide

scholarly journals Dynamics of Nitrotyrosine Formation and Decay in Rat Brain during Focal Ischemia-Reperfusion

1999 ◽  
Vol 19 (6) ◽  
pp. 667-672 ◽  
Author(s):  
Shunya Takizawa ◽  
Naoto Fukuyama ◽  
Hisayuki Hirabayashi ◽  
Hiroe Nakazawa ◽  
Yukito Shinohara
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Rat Brain ◽  
Inducible Nitric Oxide Synthase ◽  
Time Window ◽  
Ischemia Reperfusion ◽  
Late Phase ◽  
Focal Ischemia ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The purpose of this study was to establish the dynamics of nitrotyrosine (NO2-Tyr) formation and decay during the rise of NO2-Tyr in rat brain subjected to 2-hour focal ischemia-reperfusion, and to evaluate the role of inducible nitric oxide synthase in the rise. The authors first determined the half life of NO2-Tyr in rat brain at 24 hours after the start of reperfusion by blocking NO2-Tyr formation with NG-monomethyl-l-arginine and after the decay of NO2-Tyr by means of a hydrolysis/HPLC procedure. The values obtained were approximately 2 hours in both peri-infarct and core-of-infarct regions. Using the same hydrolysis/HPLC procedure, the ratio of nitrotyrosine to tyrosine from the 2-hour occlusion to as much as 72 hours after the start of reperfusion was measured in the presence and absence of aminoguanidine (100 mg/kg intraperitoneally twice a day). In the absence of aminoguanidine, the ratio of NO2-Tyr in the peri-infarct and core-of-infarct regions reached 0.95% ± 0.34% and 0.52% ± 0.34%, respectively, at 1 hour after the start of reperfusion, The elevated levels persisted until 48 hours, then declined, The peri-infarct region showed the highest percent NO2-Tyr level, followed by the core of infarct, then the caudoputamen, Aminoguanidine significantly reduced NO2-Tyr formation (up to 90% inhibition) during 24 to 48 hours, The authors conclude that inducible nitric oxide synthase is predominantly responsible for NO2-Tyr formation, at least in the late phase of reperfusion, These results have important implications for the therapeutic time window and choice of nitric oxide synthase inhibitors in patients with cerebral infarction.

scholarly journals Inducible nitric oxide synthase inhibits oxygen consumption in collateral-dependent myocardium

2014 ◽  
Vol 306 (3) ◽  
pp. H356-H362 ◽  
Author(s):  
Yingjie Chen ◽  
Ping Zhang ◽  
Jingxin Li ◽  
Xin Xu ◽  
Robert J. Bache
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Vascular Endothelial Cells ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Coordinated Expression ◽  
Collateral Vessels ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Following coronary artery occlusion growth of collateral vessels can provide an effective blood supply to the dependent myocardium. The ischemia, which results in growth of collateral vessels, recruits an inflammatory response with expression of cytokines and growth factors, upregulation of endothelial nitric oxide (NO) synthase (eNOS) in vascular endothelial cells, and expression of inducible nitric oxide synthase (iNOS) in both vessels and cardiac myocytes. Because NO is a potent collateral vessel dilator, this study examined whether NO derived from iNOS or constitutive NOS regulates myocardial blood flow (MBF) in the collateral region. Nonselective NOS inhibition with NG-nitro-l-arginine (LNA) caused vasoconstriction with a significant decrease in MBF to the collateral region during exercise. In contrast, the highly selective iNOS inhibitor 1400W caused a 21 ± 5% increase of MBF in the collateral region. This increase in MBF following selective iNOS blockade was proportionate to an increase in myocardial O2 consumption (MV̇o2). The results suggest that NO produced by iNOS inhibits MV̇o2 in the collateralized region, so that the increase in MBF following iNOS blockade was the result of metabolic vasodilation secondary to an increase in MV̇o2. Thus the coordinated expression of iNOS to restrain MV̇o2 and eNOS to maintain collateral vasodilation act to optimize the O2 supply-demand relationship and protect the collateralized myocardium from ischemia.

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