The dynamic detection of NO during stroke and reperfusion<i>in vivo</i>

Liu, Kezhou; Li, Qian; Zhang, Le; Zheng, Xiaoxiang

doi:10.1080/02699050902838173

Cited by 14 publications

(7 citation statements)

References 31 publications

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“…177 Much different NO responses have been reported for in vivo experiments using larger commercial NO electrodes (diameter ~200 μm) to measure the time course of tissue NO in rat hippocampus during ischemia and reperfusion. 178,179 A large decrease in NO was measured during ischemia, which is consistent with O 2 requirements for NO production by NOS. Baseline NO measurements were approximately 400 nM in this study, with increases in NO of between 700 and 800 nM above baseline during reperfusion.…”

Section: Soluble Guanylate Cyclase As Primary Target Of Nitric Osupporting

confidence: 72%

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Nitric Oxide Signaling in the Microcirculation

Buerk

Barbee

Jaron

2011

Crit Rev Biomed Eng

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Several apparent paradoxes are evident when one compares mathematical predictions from models of nitric oxide (NO) diffusion and convection in vasculature structures with experimental measurements of NO (or related metabolites) in animal and human studies. Values for NO predicted from mathematical models are generally much lower than in vivo NO values reported in the literature for experiments, specifically with NO microelectrodes positioned at perivascular locations next to different sizes of blood vessels in the microcirculation and NO electrodes inserted into a wide range of tissues supplied by the microcirculation of each specific organ system under investigation. There continues to be uncertainty about the roles of NO scavenging by hemoglobin versus a storage function that may conserve NO, and other signaling targets for NO need to be considered. This review describes model predictions and relevant experimental data with respect to several signaling pathways in the microcirculation that involve NO.

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Section: Soluble Guanylate Cyclase As Primary Target Of Nitric Osupporting

confidence: 72%

“…The baseline NO was not characterized in the other study, but the average peak NO increase during reperfusion was 768 nM above baseline. 179 …”

Section: Soluble Guanylate Cyclase As Primary Target Of Nitric Omentioning

confidence: 99%

Nitric Oxide Signaling in the Microcirculation

Buerk

Barbee

Jaron

2011

Crit Rev Biomed Eng

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“…Furthermore, eNOS is not only a downstream mediator for vascular endothelial growth factor and angiogenesis but also regulates brain-derived neurotrophic factor expression in the ischemic brain and influences progenitor cell proliferation, neuronal migration, and neurite outgrowth and affects functional recovery after stroke [15] . In contrast, NO derived by iNOS and nNOS contributes to the brain injury in cerebral ischemic reperfusion, in which NO interacts with superoxide anion to produce peroxynitrite [1,6,16,17] . Consistent with these principles, the effects of NOS inhibitors on infarct size in animal studies demonstrated that nonselective NOS inhibitors did not alter infarct volume in permanent ischemia, whereas selective iNOS and nNOS inhibitors reduced lesion size regardless of experimental model [1] .…”

Section: Discussionmentioning

confidence: 98%

GTP cyclohydrolase 1 gene 3′-UTR C+243T variant predicts worsening outcome in patients with first-onset ischemic stroke

Tang

Zhang

Ding

et al. 2010

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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Tetrahydrobiopterin (BH4) is an essential cofactor for all three nitric oxide synthase (NOS isoforms), which plays an important role in vascular diseases. GTP cyclohydrolase 1 (GCH 1) is the first-step and rate-limiting enzyme for BH4 biosynthesis in its de novo pathway. Common GCH1 gene variant C+243T in the 3'-untranslated region predicts NO excretion. The present study examined the predictive role of GCH 1 gene 3'-UTR C+243T variant in the long-term outcome of ischemic stroke. A total of 142 patients with first-onset ischemic stroke were recruited and detected for genotype of GCH1 3'-UTR C+243T by a TaqMan SNP Genotyping assay. Subsequent vascular events and death were determined over a 5-year follow-up period. The frequency of GCH1 3'-UTR +243 C/T or T/T genotype was significantly increased in patients with endpoint events as compared with those without events (74% vs 57.8%, P=0.06). Cox regression survival analysis indicated that an increased probability of death or new vascular events was found in patients with GCH1 3'-UTR +243 C/T or T/T genotype compared with those with GCH1 3'-UTR C/C genotype (40.6% vs 25.5%), GCH1 3'-UTR +243 C/T or T/T genotype relative to GCH1 3'-UTR C/C genotype was associated with the increased risk of death or vascular events even after adjustment for other risk factors (OR=2.171, 95% CI: 1.066-4.424, P=0.033). It was concluded that GCH1 3'-UTR C+243T variant was an independent predictor of worsening long-term outcomes in patients with first-onset ischemic stroke.

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“…However, immediately after reperfusion, biosynthesis of this molecule is triggered mainly by overactivation of nNOS, as evidenced in nNOS (−/−) mice [48] or with specific inhibitors such as 7-NI [41, 49]. Glutamate-induced Ca 2+ overload in ischemic neurons is responsible for the rise of nNOS-derived NO [50].…”

Section: Nitric Oxide Donors (Nod) As Neuroprotective Agents In Ismentioning

confidence: 99%

“…Glutamate-induced Ca 2+ overload in ischemic neurons is responsible for the rise of nNOS-derived NO [50]. Concentration of NO returns to physiological levels approximately 1 h after reperfusion [48, 49, 51] and increases again due to iNOS expression between 12 h and up to 8 days later [52, 53]. iNOS sources at this stage comprise microglia [53], astrocytes [54], endothelial cells [55], and infiltrated leukocytes [56].…”

Section: Nitric Oxide Donors (Nod) As Neuroprotective Agents In Ismentioning

confidence: 99%

Nitric Oxide Donors as Neuroprotective Agents after an Ischemic Stroke-Related Inflammatory Reaction

Godínez-Rubí

Rojas-Mayorquín

Ortuño-Sahagún

2013

Oxidative Medicine and Cellular Longevity

103

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Cerebral ischemia initiates a cascade of detrimental events including glutamate-associated excitotoxicity, intracellular calcium accumulation, formation of Reactive oxygen species (ROS), membrane lipid degradation, and DNA damage, which lead to the disruption of cellular homeostasis and structural damage of ischemic brain tissue. Cerebral ischemia also triggers acute inflammation, which exacerbates primary brain damage. Therefore, reducing oxidative stress (OS) and downregulating the inflammatory response are options that merit consideration as potential therapeutic targets for ischemic stroke. Consequently, agents capable of modulating both elements will constitute promising therapeutic solutions because clinically effective neuroprotectants have not yet been discovered and no specific therapy for stroke is available to date. Because of their ability to modulate both oxidative stress and the inflammatory response, much attention has been focused on the role of nitric oxide donors (NOD) as neuroprotective agents in the pathophysiology of cerebral ischemia-reperfusion injury. Given their short therapeutic window, NOD appears to be appropriate for use during neurosurgical procedures involving transient arterial occlusions, or in very early treatment of acute ischemic stroke, and also possibly as complementary treatment for neurodegenerative diseases such as Parkinson or Alzheimer, where oxidative stress is an important promoter of damage. In the present paper, we focus on the role of NOD as possible neuroprotective therapeutic agents for ischemia/reperfusion treatment.

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The dynamic detection of NO during stroke and reperfusionin vivo

Cited by 14 publications

References 31 publications

Nitric Oxide Signaling in the Microcirculation

Nitric Oxide Signaling in the Microcirculation

GTP cyclohydrolase 1 gene 3′-UTR C+243T variant predicts worsening outcome in patients with first-onset ischemic stroke

Nitric Oxide Donors as Neuroprotective Agents after an Ischemic Stroke-Related Inflammatory Reaction

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