Effect of focal cerebral ischemia on nitric oxide synthase expression in rats

1997 ◽  
Vol 30 (2) ◽  
pp. 55-62 ◽  
Author(s):  
Hideki Homma ◽  
Hidekatsu Mizushima ◽  
Yoshinori Arai ◽  
Kenji Dohi ◽  
Kiyoshi Matsumoto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Nitric Oxide Synthase ◽  
Focal Cerebral Ischemia ◽  
Oxide Synthase

Effects of Inhibition of Nitric Oxide Synthase on Blood-Brain Barrier Transport in Focal Cerebral Ischemia

Pharmacology ◽  
1994 ◽  
Vol 48 (6) ◽  
pp. 367-373 ◽  
Author(s):  
Oak Za Chi ◽  
Hwu Meei Wei ◽  
Arabinda K. Sinha ◽  
Harvey R. Weiss
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Nitric Oxide Synthase ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Oxide Synthase

scholarly journals Functional Deterioration of Endothelial Nitric Oxide Synthase after Focal Cerebral Ischemia

2013 ◽  
Vol 33 (10) ◽  
pp. 1532-1539 ◽  
Author(s):  
Yoshiki Yagita ◽  
Kazuo Kitagawa ◽  
Naoki Oyama ◽  
Toshiro Yukami ◽  
Akihiro Watanabe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Focal Cerebral Ischemia ◽  
Rho Kinase ◽  
Ischemic Lesion ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Functional Deterioration

Endothelial nitric oxide synthase (eNOS) dysfunction is related to secondary injury and lesion expansion after cerebral ischemia. To date, there are few reports about postischemic alterations in the eNOS regulatory system. The purpose of the present study was to clarify eNOS expression, Ser1177 phosphorylation, and monomer formation after cerebral ischemia. Male Wistar rats were subjected to transient focal cerebral ischemia. Endothelial nitric oxide synthase messenger RNA (mRNA) and protein expression increased ~ 8-fold in the ischemic lesion. In the middle cerebral artery core, eNOS-Ser1177 phosphorylation increased 6 hours after ischemia; however, there was an approximately 90% decrease in eNOS-Ser1177 phosphorylation observed 24 hours after ischemia that continued until at least 7 days after ischemia. Endothelial nitric oxide synthase monomer formation also increased 24 and 48 hours after ischemia ( P<0.05), and protein nitration progressed in parallel with monomerization. To assess the effect of a neuroprotective agent on eNOS dysfunction, we evaluated the effect of fasudil, a Rho-kinase inhibitor, on eNOS phosphorylation and dimerization. Postischemic treatment with fasudil suppressed lesion expansion and dephosphorylation and monomer formation of eNOS. In conclusion, functional deterioration of eNOS progressed after cerebral ischemia. Rho-kinase inhibitors can reduce ischemic lesion expansion as well as eNOS dysfunction in the ischemic brain.

Ghrelin Suppresses Inflammation and Neuronal Nitric Oxide Synthase in Focal Cerebral Ischemia Via the Vagus Nerve

Shock ◽  
2011 ◽  
Vol 35 (3) ◽  
pp. 258-265 ◽  
Author(s):  
Cletus Cheyuo ◽  
Rongqian Wu ◽  
Mian Zhou ◽  
Asha Jacob ◽  
Gene Coppa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Nitric Oxide Synthase ◽  
Vagus Nerve ◽  
Focal Cerebral Ischemia ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase

Effect of intermittent reperfusion and nitric oxide synthase inhibition on infarct volume during reversible focal cerebral ischemia

1995 ◽  
Vol 83 (3) ◽  
pp. 491-495 ◽  
Author(s):  
Brian A. Iuliano ◽  
Robert E. Anderson ◽  
Fredric B. Meyer
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Nitric Oxide Synthase ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Vascular Occlusion ◽  
Artery Occlusion ◽  
Content Type ◽  
Infarction Size ◽  
Oxide Synthase

✓ The authors examined the effects of both intermittent reperfusion and nitric oxide synthase (NOS) inhibition, caused by NG-nitro-l-arginine methyl ester (l-NAME) during episodes of focal cerebral ischemia induced to simulate the neurosurgical setting. Seventy-eight Wistar rats underwent single (60 minutes of ischemia) or repetitive (four 15-minute periods of ischemia separated by 5 minutes of reperfusion) episodes of middle cerebral artery occlusion while under anesthesia (1.0% halothane). Twenty-four hours after the procedure, the animals were given neurological examinations and then sacrificed for histological preparation and examination. The intermittent reperfusion groups tended to have smaller mean cortical infarctions. There was also a trend showing a decrease in infarction size in groups given l-NAME. The combination of intermittent reperfusion and preischemic administration ofl-NAME (10 mg/kg) resulted in a 65% reduction in infarction size (p < 0.05) when compared to that caused by 60 minutes of single occlusion without l-NAME. The use of NOS inhibition combined with intermittent reperfusion may be a technique to provide intraoperative cerebral protection during neurovascular procedures that require temporary vascular occlusion.

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