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Amitriptyline administration transforms tumor necrosis factor-alpha regulation of norepinephrine release in the brain.

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The present study demonstrates that the mixed action antidepressant drug amitriptyline enhances norepinephrine (NE) release by transforming the nature of the response of neurons to both tumor necrosis factor-alpha (TNF) as well as to an alpha(2)-adrenergic agonist in an area of the central nervous

Antinociception mediated by alpha(2)-adrenergic activation involves increasing tumor necrosis factor alpha (TNFalpha) expression and restoring TNFalpha and alpha(2)-adrenergic inhibition of norepinephrine release.

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The central component that establishes chronic pain from peripheral nerve injury is associated with increased tumor necrosis factor-alpha (TNFalpha) production in the brain. This study examined TNFalpha and its reciprocally permissive role with alpha(2)-adrenergic activation during peak and

Bilateral toe necrosis resulting from norepinephrine bitartrate usage.

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Acute limb ischemia may manifest by ischemic rest pain, ischemic ulcers, or gangrene. Acute arterial occlusion can be the result of emboli from a distant source, acute thrombosis of a previously patent artery, or direct trauma to an artery. Toe necrosis resulting from norepinephrine bitartrate

The toxicity of tumor necrosis factor-alpha upon cholinergic neurons within the nucleus basalis and the role of norepinephrine in the regulation of inflammation: implications for Alzheimer's disease.

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Inflammation and reduced forebrain norepinephrine are features of Alzheimer's disease that may interact to contribute to the degeneration of specific neural systems. We reproduced these conditions within the basal forebrain cholinergic system, a region that is vulnerable to degeneration in

Sequential release of leukotrienes and norepinephrine in rat bowel after platelet-activating factor. A mechanistic study of platelet-activating factor-induced bowel necrosis.

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We have developed a model of ischemic bowel necrosis in the rat by injecting synthetic platelet-activating factor into the mesenteric vascular bed. Our previous studies have shown that the development of ischemic necrosis was not due to thrombus formation, but to release of vasoconstricting

Tumor necrosis factor and norepinephrine lower the levels of human neutrophil peptides 1-3 secretion by mixed synovial tissue cultures in osteoarthritis and rheumatoid arthritis.

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BACKGROUND Neutrophils and monocytes play an important role in overt inflammation in chronic inflammatory joint diseases such as rheumatoid arthritis (RA). The sympathetic nervous system (SNS) inhibits many neutrophil/monocyte functions and macrophage tumor necrosis factor (TNF), but because of the

Hepatic necrosis induced by norepinephrine in rabbits.

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Extensive hepatic necrosis was produced in rabbits 48 hr following infusion of a cardiopathogenic dose of norepinephrine (NE, 2 micrograms/kg/min for 90 min). Livers had necrotic areas of varying sizes and gross appearances. Histologically, the lesions were areas of varying sizes and gross

Preferential Protection of Cerebral Autoregulation and Reduction of Hippocampal Necrosis With Norepinephrine After Traumatic Brain Injury in Female Piglets.

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OBJECTIVE Traumatic brain injury contributes to morbidity in children and boys is disproportionately represented. Cerebral autoregulation is impaired after traumatic brain injury, contributing to poor outcome. Cerebral perfusion pressure is often normalized by the use of vasopressors to increase

Norepinephrine is a more potent inhibitor of tumor necrosis factor over a range of doses than dopamine.

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In the current study, we test the hypothesis that norepinephrine has greater anti-inflammatory effects versus dopamine over a range of doses in a model of lipopolysaccharide (LPS)-stimulated cytokine release in human saphenous vein. Segments of saphenous vein were cut and separated into 1 mm x 1 mm

Ischemic Necrosis of Upper Lip, and All Fingers and Toes After Norepinephrine Use.

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A 68-year-old woman with necrosis of total finger, toe, and upper lip was requested by department of internal medicine. She was diagnosed with septic shock and treated with norepinephrine 10 days ago. Norepinephrine is an often-used medicine for normalizing blood pressure in septic shock patients.

Effect of tumor necrosis factor-alpha on the reciprocal G-protein-induced regulation of norepinephrine release by the alpha2-adrenergic receptor.

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Alpha2-adrenergic receptors control norepinephrine (NE) release and tumor necrosis factor-alpha (TNF) production from neurons. TNF regulates NE release, depending on alpha2-adrenergic receptor functioning. The relationship between TNF production in the brain and alpha2-adrenergic receptor activation

Hypothalamic corticotrophin-releasing factor and norepinephrine mediate sympathetic and cardiovascular responses to acute intracarotid injection of tumour necrosis factor-alpha in the rat.

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Systemic administration of tumour necrosis factor (TNF)-alpha induces the release of norepinephrine in the paraventricular nucleus (PVN) of hypothalamus and an increase in expression of corticotrophin-releasing factor (CRF) and CRF type 1 receptors. We explored the hypothesis that CRF and

Daily light and darkness onset and circadian rhythms metabolically synchronize hematopoietic stem cell differentiation and maintenance: The role of bone marrow norepinephrine, tumor necrosis factor, and melatonin cycles.

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Hematopoietic stem and progenitor cells (HSPCs) are essential for daily mature blood cell production, host immunity, and osteoclast-mediated bone turnover. The timing at which stem cells give rise to mature blood and immune cells while maintaining the bone marrow (BM) reservoir of undifferentiated

Mechanism underlying tumor necrosis factor-alpha suppression of norepinephrine release from rat myenteric plexus.

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We studied the effect of tumor necrosis factor-alpha (TNF-alpha) on the release of [3H]norepinephrine ([3H]NE) from longitudinal muscle-myenteric plexus preparations of rat jejunum. TNF-alpha had no immediate effect on [3H]NE release. Preincubation of the tissue with TNF-alpha caused a suppression

Mouse tumor necrosis factor-alpha increases brain tryptophan concentrations and norepinephrine metabolism while activating the HPA axis in mice.

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Endotoxin (LPS) administration has been shown to activate the hypothalamo-pituitary-adrenocortical (HPA) axis and increase cerebral catecholamine and indolamine metabolism and tryptophan concentrations. LPS stimulates the secretion of tumor necrosis factor-alpha (TNF-alpha) as well as interleukin-1

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