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ethanolamine/nekrose
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Extensive necrosis of duodenum after injection sclerotherapy of a bleeding duodenal ulcer with 5% ethanolamine.
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Inhibition of tumor necrosis factor-alpha improves postischemic recovery of hypertrophied hearts.
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BACKGROUND
Tumor necrosis factor (TNF)-alpha has been implicated in the pathogenesis of heart failure and ischemia-reperfusion injury. Effects of TNF-alpha are initiated by membrane receptors coupled to sphingomyelinase signaling and include altered metabolism and calcium cycling, contractile
A Complication of Percutaneous Sclerotherapy for Congenital Pulmonary Airway Malformation: Intravascular Injection and Cardiac Necrosis.
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BACKGROUND
A congenital pulmonary airway malformation (CPAM) type III may become large enough to cause hydrops fetalis. In such circumstances, the fetus can be treated with open fetal resection, maternal betamethasone administration, or percutaneous sclerotherapy.
METHODS
A 24 week gestation fetus
A comparison of sclerosing agents. Clinical and histologic effects of intravascular sodium morrhuate, ethanolamine oleate, hypertonic saline (11.7%), and sclerodex in the dorsal rabbit ear vein.
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The dorsal marginal rabbit ear vein was injected with 0.25 mL of 2.5, 1, or 0.5% sodium morrhuate, 2.5, 1, or 0.5% ethanolamine oleate, hypertonic saline 11.7%, or Sclerodex. Only the vessel injected with 2.5% sodium morrhuate demonstrated clinical and histologic evidence of endosclerosis with
An experimental study on hepatotoxicity of sclerosant ethanolamine oleate flowed into portal vein.
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Although endoscopic injection sclerotherapy has been a main treatment option for gastroesophageal varices, intraportal inflow of the sclerosant, ethanolamine oleate, induce liver damage. The aim of this study was to clarify the liver damage due to intraportal inflow of ethanolamine oleate.
N-Trifluoroacetyl-ethanolamine: a proposed urinary metabolite of halothane: validation and measurement in children.
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It has been postulated that trifluoroacetyl chloride, a halothane metabolite, can bind covalently with the phosphatidylethanolamine component of the hepatic cell membrane and cause cell necrosis. Breakdown of the necrotic hepatocyte would release N-trifluoroacetyl-ethanolamine (TFAE) into the serum
Injection of ethanolamine oleate into a segmental portal branch for pharmacologic hepatic segmentectomy in dogs.
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OBJECTIVE
Currently available treatments for hepatocellular carcinoma are not satisfactory in terms of recurrence rates. In this study, we injected ethanolamine oleate (EO) into a portal branch in an attempt to cause necrosis of a liver segment in which hepatocellular carcinoma might be
Two models of acute hepatic failure with extensive hepatic necrosis and blood ammonia elevation in small animals.
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Acute hepatic failure models with extensive hepatic necrosis and hyperammonemia were developed in small animals. One model is bases on the retrograde infusion of ethanolamine oleate into the common bile duct of guinea pigs and another is based on the infusion of TNF-lipiodol emulsion into the portal
Resistance to killing by tumor necrosis factor in an adipocyte cell line caused by a defect in arachidonic acid biosynthesis.
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We have found that TA1-R6, which are resistant to the cytotoxic effects of tumor necrosis factor (TNF) in the presence of cycloheximide (Reid, T. R., Torti, F., and Ringold, G. M. (1989) J. Biol. Chem. 264, 4583-4589), have reduced ability to release arachidonic acid (20:4) from membrane
Role of ethanolamine phosphate in the hippocampus of rats with acute experimental autoimmune encephalomyelitis.
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Here, we assessed the effects of acute experimental autoimmune encephalomyelitis (EAE) on the rat hippocampal somatostatinergic system and whether administration of an ethanolamine phosphate salt could prevent the appearance of the clinical signs and the impairment of the somatostatinergic system in
Characterisation of the prostaglandin E2-ethanolamide suppression of tumour necrosis factor-α production in human monocytic cells.
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OBJECTIVE
Prostaglandin ethanolamides or prostamides are naturally occurring neutral lipid derivatives of prostaglandins that have been shown to be synthesised in vivo following COX-facilitated oxygenation of arachidonoyl ethanolamine (anandamide). Although the actions of prostaglandins have been
Hemodynamic and morphological changes in the dog kidney after injection of 5% ethanolamine oleate into the superior vena cava.
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The effect of the sclerosant 5% ethanolamine oleate (EO) on renal circulation was evaluated in 20 mongrel dogs into which we injected 5% EO (0.5 ml/kg) into the superior vena cava. There was a marked hemolysis and a significant decrease in creatinine clearance from 104.4 +/- 17.1 (mean +/- SD) to
Effects of tumour necrosis factor α upon the metabolism of the endocannabinoid anandamide in prostate cancer cells.
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Tumour necrosis factor α (TNFα) is involved in the pathogenesis of prostate cancer, a disease where disturbances in the endocannabinoid system are seen. In the present study we have investigated whether treatment of DU145 human prostate cancer cells affects anandamide (AEA) catabolic pathways.
Non-clinical safety evaluation of a novel pharmaceutical salt, rosuvastatin ethanolamine, in Wistar rats.
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Rosuvastatin, a second generation 3-Hydroxy-3-Methyl Glutaryl Coenzyme-A reductase inhibitor, is widely used for the management of hypercholesterolemia. Rosuvastatin ethanolamine, developed by Cadila Healthcare Ltd., is a novel, chemically stable, and pharmaceutically acceptable salt, having better
Metabolic profiling predicts response to anti-tumor necrosis factor α therapy in patients with rheumatoid arthritis.
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OBJECTIVE
Anti-tumor necrosis factor (anti-TNF) therapies are highly effective in rheumatoid arthritis (RA) and psoriatic arthritis (PsA), but a significant number of patients exhibit only a partial or no therapeutic response. Inflammation alters local and systemic metabolism, and TNF plays a role
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