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d tubocurarine/necrosis

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8 結果
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
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
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
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
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
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
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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