Bench to Bedside Nitric Oxide in Emergency Medicine

Lopez, Bernard L.; Christopher, Theodore A.; Griswold, Sharon; Liang, Xuefang

doi:10.1111/j.1553-2712.2000.tb01081.x

Cited by 8 publications

(16 citation statements)

References 101 publications

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“…NO production is catalyzed by 3 isoforms of NO synthase (NOS): endothelial or eNOS by vascular endothelium in the cardiovascular system, neuronal or nNOS, primarily operational in producing NO as a neurotransmitter, and inducible or iNOS, produced by a variety of cells (endothelial and otherwise) for a variety of reasons, including an immune-mediated or inflammatory response [6]. Both the calcium dependent NOSs (eNOS and nNOS), have transient activities and thus exhibit relatively low concentrations, usually ranging in the nM range, while the cytokine activated, calcium independent, iNOS is long lasting, generating higher concentrations of NO, usually in the µM range [6]. As a vascular effector, NO rapidly diffuses from its site of generation in endothelial cells into adjacent smooth muscle cells, where it activates soluble guanylate cyclase (Fig.…”

Section: Nitric Oxide and Its Metabolites: Physiological And Biochemimentioning

confidence: 99%

“…During fasting conditions with low dietary intake of NOx, enzymatic formation of NO via NOS accounts for the majority of circulating NOx. Nitrate and nitrite have been shown to be biomarkers for cardiovascular and other diseases from both diagnostic and therapeutic aspects [6, 8]. In addition to blood, urinary levels of NOx provide a means to assess systemic production of NO in vivo , however, with the caveat that urinary (or plasma) levels are truly reflective of endogenous production of NO, dietary ingestion of NOx, as well as from bacterial activity in the gut [6, 8].…”

Section: Nitric Oxide and Its Metabolites: Physiological And Biochemimentioning

confidence: 99%

See 1 more Smart Citation

Nitric Oxide and its Metabolites in the Critical Phase of Illness: Rapid Biomarkers in the Making

Mian

Aranke²,

Bryan

2013

Open Biochem J

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The potential of nitric oxide (NO) as a rapid assay biomarker, one that could provide a quantum leap in acute care, remains largely untapped. NO plays a crucial role as bronchodilator, vasodilator and inflammatory mediator. The main objective of this review is to demonstrate how NO is a molecule of heavy interest in various acute disease states along the emergency department and critical care spectrum: respiratory infections, central nervous system infections, asthma, acute kidney injury, sepsis, septic shock, and myocardial ischemia, to name just a few. We discuss how NO and its oxidative metabolites, nitrite and nitrate, are readily detectable in several body compartments and fluids, and as such they are associated with many of the pathophysiological processes mentioned above. With methods such as high performance liquid chromatography and chemiluminescence these entities are relatively easy and inexpensive to analyze. Emphasis is placed on diagnostic rapidity, as this relates directly to quality of care in acute care situations. Further, a rationale is provided for more bench, translational and clinical research in the field of NO biomarkers for such settings. Developing standard protocols for the aforementioned disease states, centered on concentrations of NO and its metabolites, can prove to revolutionize diagnostics and prognostication along a spectrum of clinical care. We present a strong case for developing these biomarkers more as point-of-care assays with potential of color gradient test strips for rapid screening of disease entities in acute care and beyond. This will be relevant to global health.

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Section: Nitric Oxide and Its Metabolites: Physiological And Biochemimentioning

confidence: 99%

Section: Nitric Oxide and Its Metabolites: Physiological And Biochemimentioning

confidence: 99%

Nitric Oxide and its Metabolites in the Critical Phase of Illness: Rapid Biomarkers in the Making

Mian

Aranke²,

Bryan

2013

Open Biochem J

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“…Inhibition of NO synthase (NOS) prevents the myocardial depressive effects of either TNF or IL-1, suggesting that the negative inotropic effects of TNF are mediated by NO. 35,36 Lipopolysaccharide, TNF, and IL-1 each induce NOS and augment guanosine 38,58-cyclic monophosphate, which mediates NO's effects in a number of cell types. 35,36 Nitric oxide also mediates TNF-induced desensitization of myofilaments to increased intracellular calcium.…”

Section: 34mentioning

confidence: 99%

“…35,36 Lipopolysaccharide, TNF, and IL-1 each induce NOS and augment guanosine 38,58-cyclic monophosphate, which mediates NO's effects in a number of cell types. 35,36 Nitric oxide also mediates TNF-induced desensitization of myofilaments to increased intracellular calcium. 37 While several investigators have implicated NO in TNF-induced myocardial dysfunction, 10,35,41 others have not attributed all of TNF's contractile depression to NO.…”

Section: 34mentioning

confidence: 99%

Bench to Bedside Tumor Necrosis Factor‐alpha: From Inflammation to Resuscitation

Cairns

Panacek

Harken

et al. 2000

Academic Emergency Medicine

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Abstract. Proinflammatory mediators such as tumor necrosis factor-alpha (TNF) have been implicated in the pathophysiology in a number of acute disease states. Tumor necrosis factor-alpha can contribute to cell death, apoptosis, and organ dysfunction. Tumor necrosis factor-alpha can be generated with sepsis or ischemia-reperfusion by activation of cell mitogen-activated protein kinases and nuclear factor kappa B, leading to TNF production. A number of strategies to modulate TNF have been recently explored, including factors directed toward mitogen-activated protein kinases, TNF transcription, anti-inflammatory ligands, heat shock proteins, and TNF-binding proteins. However, TNF may also play an important role in the adaptive response to injury and inflammation. Control of the deleterious effects of TNF and other proinflamatory cytokines represents a realistic goal for clinical emergency medicine. The purpose of this article is to provide a background of relevance to emergency medicine academicians on the production and regulation of TNF, the acute effects of TNF on pathophysiology, and the rationale for therapeutic interventions directed toward TNF and the clinical experience with these strategies. Key words: sepsis; shock; ischemia and reperfusion; therapy; trauma; emergency; review; tumor necrosis factor. ACA-DEMIC EMERGENCY MEDICINE 2000; 7:930-941 I NFLAMMATORY cytokines are known to be important mediators of numerous disease states faced by emergency physicians.1-8 A basic understanding of inflammatory cytokines and their relationship to acute disease is of growing importance to laboratory scientists, clinical researchers, and clinicians. Tumor necrosis factor-alpha (TNF) is a proinflammatory cytokine that has been directly implicated in the pathogenesis of many acute disease states, including sepsis, traumatic injury, cardiac and cerebral ischemia, asthma, and burns. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] Tumor necrosis factor-alpha may also play an important role in the adaptive response to injury and inflammation. 14 The intracellular signal pathways that provoke TNF production have been the subject of intense investigations. 10,17,18 In particular, the discovery of Other therapeutic targets include the activation of endogenous anti-inflammatory strategies such as ligands for the gp130 subunit, the induction of heat shock proteins (HSPs), and infusion of TNF-binding proteins. These approaches hold the promise of directly modulating the destructive role of proinflammatory cytokines, such as TNF, in acute disease states.The purpose of this article is to provide a background of relevance to emergency medicine academicians on the production and regulation of TNF, the acute effects of TNF on pathophysiology, and the rationale for therapeutic interventions directed toward TNF and the clinical experience with these strategies.

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“…1 Generally, these would be topics more often seen in the basic research journals, and not well known to the majority of the AEM readership. Yet the application of these basic approaches may very well impact EM research, education, and clinical practice.…”

mentioning

confidence: 99%

The Emergency Physician as Integrative Physiologist Inauguration of the Academic Emergency Medicine “Bench to Bedside” Series

Panacek

Cairns

2000

Academic Emergency Medicine

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Bench to Bedside Nitric Oxide in Emergency Medicine

Cited by 8 publications

References 101 publications

Nitric Oxide and its Metabolites in the Critical Phase of Illness: Rapid Biomarkers in the Making

Nitric Oxide and its Metabolites in the Critical Phase of Illness: Rapid Biomarkers in the Making

Bench to Bedside Tumor Necrosis Factor‐alpha: From Inflammation to Resuscitation

The Emergency Physician as Integrative Physiologist Inauguration of the Academic Emergency Medicine “Bench to Bedside” Series

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