tubocurarine/necroză

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Effects of human recombinant IL-1 on d-tubocurarine-induced histamine release from isolated rat peritoneal mast cells.

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The relationship between d-tubocurarine (d-Tc) and human recombinant interleukin-1 (rIL-1) was studied on the histamine-releasing property of isolated rat peritoneal mast cells. d-Tc induced histamine release in a dose-dependent manner (1 x 10(-4) M-3 x 10(-3) M) from isolated rat mast cells. Human

Bay K 8644 induced necrosis in murine skeletal muscle in vitro: myofibre breakdown precedes significant alterations of intracellular [Ca] or pH.

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The effect of the Ca2+-channel agonist Bay K 8644 (1 mumol/l) on the ultrastructure, Ca2+-homeostasis, pH and membrane potential of murine diaphragm muscle, in vitro, has been investigated. Treatment with Bay K 8644 in a standard physiological saline, for 1-2 h, induced swelling of the muscle

Prevention of phospholine-induced myopathy with d-tubocurarine, atropine sulfate, diazepam, and creatine phosphate.

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Acute administration of phospholine [diethyl-S-(2-dimethyl aminoethyl)phosphorothioate] at 0.2 mg/kg sc produces a myopathy characterized by initial focal changes in the subsynaptic area of the skeletal muscle. The onset of the myopathy is associated with fasciculations of high frequency. Agents

Diisopropylphosphorofluoridate-induced cholinergic hyperactivity and lipid peroxidation.

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In the present study, the association between acetylcholine (ACh)-induced muscle necrosis and the appearance of lipid peroxidation products was investigated. Lipid peroxidation in this injury was quantified by the malondialdehyde-thiobarbituric acid complex (TBA-MDA) using HPLC. To induce muscle

Lipid peroxidation and changes in cytochrome c oxidase and xanthine oxidase activity in organophosphorus anticholinesterase induced myopathy.

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A possible role of radical oxygen species (ROS) initiated lipid peroxidation in diisopropylphosphorofluoridate (DFP)-induced muscle necrosis was investigated by quantifying muscle changes in F2-isoprostanes, novel and extremely accurate markers of lipid peroxidation in vivo. A significant increase

Nicotine modulation of apoptosis in human coronary artery endothelial cells.

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It has been recently reported that nicotine, the addictive component of tobacco, is an important modulator at the level of immune cell apoptosis or programmed cell death. Apoptosis is a process that helps maintain the homeostasis of the vascular endothelium and vascular smooth muscle cells, and

Modulation of intracellular Ca2+ levels by Scorpaenidae venoms.

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The crude venoms of the soldierfish (Gymnapistes marmoratus), the lionfish (Pterois volitans) and the stonefish (Synanceia trachynis) display pronounced neuromuscular activity. Since [Ca(2+)](i) is a key regulator in many aspects of neuromuscular function we sought to determine its involvement in

Diisopropylphosphorofluoridate-induced muscle hyperactivity associated with enhanced lipid peroxidation in vivo.

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Acute exposure to acetylcholinesterase (AChE) inhibitors such as organophosphates and carbamates induces functional changes at the neuromuscular junctions, leading to fasciculations that ultimately cause muscle fiber necrosis. There is recent evidence that oxygen free radical formation may be a

Prevention of diisopropylphosphorofluoridate (DFP)-induced skeletal muscle fiber lesions in rat.

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The objective of the present investigation was to assess the comparative efficacy of prophylactic treatment with d-tubocurarine (d-TC) (0.075 mg/kg), atropine sulfate (16 mg/kg), and atropine methylnitrate (16 mg/kg), employed singly or in combination against the diisopropylphosphorofluoridate

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