Real-time monitoring of nitric oxide in ischemic myocardium using an NO-selective electrode calibrated by electron spin resonance

Takahashi, Shunsuke; Omori, Yoichi; Miyazaki, Hiroyuki; Yoshino, Fumihiko; Shoji, Hirofumi; Lee, Masaichi-Chang-il; Todoki, Kazuo; Kamibayashi, Masato; Murakami, Eiichi

doi:10.1016/j.lfs.2003.06.027

Cited by 9 publications

(6 citation statements)

References 33 publications

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“…9,[31][32][33][34][35] Although early indirect studies reported a lack of NO production in the postischemic heart, subsequent direct measurements demonstrated that NO production is markedly increased during ischemia and the early minutes of reperfusion. 6,8,9,12,31 The present study supports the concept that eNOS-derived NO in postischemic myocardium could increase to a pathological level for some time and induce a significant inhibition of oxygen consumption. The sharp peak of myocardial PO 2 during the early minutes of reperfusion strongly suggests a transient reversible inhibition of oxygen consumption by eNOS-derived NO in wild-type mice.…”

Section: Discussionsupporting

confidence: 87%

“…3,4 Endothelial dysfunction has been demonstrated after ischemia/reperfusion in the coronary circulation, which has been attributed to a decrease in eNOS-derived NO. [5][6][7] However, increased NO formation during ischemia or the early period of reperfusion has also been shown to occur in hearts subjected to global ischemia by our laboratory and others. 8 -12 eNOS-derived NO has been reported to regulate oxygen consumption in vitro, 13,14 but controversy remains about the role of NO in regulating oxygen consumption in vivo under normal physiological conditions.…”

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confidence: 98%

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Endothelium-Derived Nitric Oxide Regulates Postischemic Myocardial Oxygenation and Oxygen Consumption by Modulation of Mitochondrial Electron Transport

et al. 2005

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Background-Nitric oxide (NO) production is increased in postischemic myocardium, and NO can control mitochondrial oxygen consumption in vitro. Therefore, we investigated the role of endothelial NO synthase (eNOS)-derived NO on in vivo regulation of oxygen consumption in the postischemic heart. Methods and Results-Mice were subjected to 30 minutes of coronary ligation followed by 60 minutes of reperfusion.Myocardial oxygen tension (PO 2 ) was monitored by electron paramagnetic resonance oximetry. In wild-type, N-nitro-L-arginine methyl ester (L-NAME)-treated (with 1 mg/mL in drinking water), and eNOS knockout (eNOS Ϫ/Ϫ ) mice, no difference was observed among baseline myocardial PO 2 values (8.6Ϯ0.7, 10.0Ϯ1.2, and 10.1Ϯ1.2 mm Hg, respectively) or those measured at 30 minutes of ischemia (1.4Ϯ0.6, 2.3Ϯ0.9, and 3.1Ϯ1.4 mm Hg, respectively). After reperfusion, myocardial PO 2 increased markedly (PϽ0.001 versus baseline in each group) but was much lower in L-NAME-treated and eNOS Ϫ/Ϫ mice (17.4Ϯ1.6 and 20.4Ϯ1.9 mm Hg) than in wild-type mice (46.5Ϯ1.7 mm Hg; PϽ0.001). A transient peak of myocardial PO 2 was observed at early reperfusion in wild-type mice. No reactive hyperemia was observed during early reperfusion. Endothelial NO decreased the rate-pressure product (PϽ0.05), upregulated cytochrome c oxidase (CcO) mRNA expression (PϽ0.01) with no change in CcO activity, and inhibited NADH dehydrogenase (NADH-DH) activity (PϽ0.01) without alteration of NADH-DH mRNA expression. Peroxynitrite-mediated tyrosine nitration was higher in hearts from wild-type mice than in eNOS Ϫ/Ϫ or L-NAME-treated hearts. Conclusions-eNOS-derived

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Section: Discussionsupporting

confidence: 87%

mentioning

confidence: 98%

Endothelium-Derived Nitric Oxide Regulates Postischemic Myocardial Oxygenation and Oxygen Consumption by Modulation of Mitochondrial Electron Transport

et al. 2005

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“…Mechanism of the cancer cell specificity for the EMW is still unclear. According to our preliminary in vitro study, we measured nitric oxide (NO) by using precision NO measuring system (InterMedical Corp., Tokyo, Japan) with NO meter (NO-501), a counter electrode (NOR-20) and a working electrode (NOE-47), before and after the EMW irradiation in W-38 cells and H322 NSCLC cells (19). In contrast to WI-38, which showed no sign of NO generation from the cell culture wells after the EMW irradiation, simultaneous surge of NO was detected in H322 wells immediately after the EMW irradiation (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of systemic external microwave hyperthermia for treatment of pleural metastasis in orthotopic lung cancer model

et al. 2010

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Abstract. External microwave (EMW) hyperthermia system (2.45 GHz wave frequency) was evaluated by in vitro studies and in vivo pleural metastasis animal model. Three different non-small-cell lung cancer cells and normal fibroblast cells (control) were treated once a day for 3 days with the prototype EMW system applying mild (39˚C), moderate (43˚C), and severe (47˚C) hyperthermia. On Day-4, tested cells were retrieved and examined by apoptosis assay kit and Western blot analysis. Cancer cells treated with moderate hyperthermia showed significant apoptosis; yet no major damage was observed to normal fibroblast cells. Western blot analysis indicated cleavage on caspase-3, -9 and PARP. Also in the cell cycle analysis, increase of sub G0-G1 population was identified. After optimization of the heating intensity for in vivo environment, we created pleural metastatic animal model in 24 immune deficiency mice (male nu/nu mice) to evaluate inhibitory effect of systemic EMW hyperthermia for disseminated tumor growth. Out of 24 mice, 8 received mild and 8 received moderate hyperthermia, and remaining 8 were the no treatment control. Whole chest area of the experimental animals was irradiated 3 times a week for 2 weeks (total of 6 time irradiations). No significant adverse event was observed including abnormal weight loss, skin burn, ulceration, and death. Metastasized tumors around the pleura and chest cavity were 75% reduced in size and weight compared to non-treated control group. Harvested tumors were stained and TUNEL assay demonstrated significant apoptosis in a moderate hyper-thermia group. The EMW hyperthermia system may be possible alternative tool as a systemic hyperthermia therapy in severely advanced lung cancer patients. Further study is necessary to determine device safeness, efficacy, and synergistic effect to other possible combination therapies.

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“…Several methods exist for directly measuring NO including electron paramagnetic resonance spectroscopy [21], chemiluminescence [22], fluorescence [23,24], and electrochemical sensing [17,25,26]. Of these approaches, miniaturized electrochemical (e.g., amperometric and voltammetric) sensors represent the most promising means for determining the spatial and temporal distributions of NO near its physiological source [17].…”

Section: Direct Methods (Nitric Oxide Sensor)mentioning

confidence: 99%

Real-Time Monitoring of Nitric Oxide Dynamics in the Myocardium: Biomedical Application of Nitric Oxide Sensor

Lee¹,

Lee²,

Park³

2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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Nitric oxide (NO) is an important physiological mediator that regulates a wide range of cellular processes in many tissues. Therefore, the accurate and reliable measurement of physiological NO concentration is essential to the understanding of NO signaling and its biological role. Most methods used for NO detection are indirect including spectroscopic approaches such as the Griess assay for nitrite and detection of methemoglobin after NO reaction with oxyhemoglobin. These methods cannot accurately reflect the changes in NO concentration in vivo and in real time. Therefore, direct methods are necessary for investigating biological process and diseases related to NO in biological conditions. There is a growing interest in the development of electrochemically based sensors for direct, in vivo, and real-time monitoring of NO. Electrochemical methods offer simplicity, good sensitivity, high selectivity, fast response times, and long-term calibration stability compared to other techniques including electron paramagnetic resonance, chemiluminescence, and fluorescence. In this article, we present real-time NO dynamics in the myocardium during myocardial ischemia-reperfusion (IR) utilizing electrochemical NO microsensor. And applications of electrochemical NO sensor for the evaluation of cardioprotective effects of therapeutic treatments such as drug administration and ischemic preconditioning are reviewed.

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Real-time monitoring of nitric oxide in ischemic myocardium using an NO-selective electrode calibrated by electron spin resonance

Cited by 9 publications

References 33 publications

Endothelium-Derived Nitric Oxide Regulates Postischemic Myocardial Oxygenation and Oxygen Consumption by Modulation of Mitochondrial Electron Transport

Endothelium-Derived Nitric Oxide Regulates Postischemic Myocardial Oxygenation and Oxygen Consumption by Modulation of Mitochondrial Electron Transport

Evaluation of systemic external microwave hyperthermia for treatment of pleural metastasis in orthotopic lung cancer model

Real-Time Monitoring of Nitric Oxide Dynamics in the Myocardium: Biomedical Application of Nitric Oxide Sensor

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