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Depressants
Published in Bev-Lorraine True, Robert H. Dreisbach, Dreisbach’s HANDBOOK of POISONING, 2001
Bev-Lorraine True, Robert H. Dreisbach
These compounds appear to block neuromuscular transmission by either of two methods. The curare derivatives and gallamine triethiodide paralyze muscles by increasing the resistance of the muscle to depolarization by the acetylcholine released by nerve stimulation. By giving neostigmine or edrophonium the resistance to depolarization can be partially overcome and the paralysis relieved. Atropine is ordinarily given along with neostigmine to block the effects of neostigmine on other systems. On the other hand, decamethonium bromide and succinylcholine chloride act by depolarizing the muscles, and no drugs are available that will overcome the paralysis thus induced. All of the skeletal neuromuscular blocking agents also depress autonomic ganglia to some extent, leading to fall in blood pressure.
Dyhidro-β-agarofurans natural and synthetic as acetylcholinesterase and COX inhibitors: interaction with the peripheral anionic site (AChE-PAS), and anti-inflammatory potentials
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Julio Alarcón-Enos, Evelyn Muñoz-Núñez, Margarita Gutiérrez, Soledad Quiroz-Carreño, Edgar Pastene-Navarrete, Carlos Céspedes Acuña
AChE has been recognised as a target for a number of toxins and promising drugs such as huperzine32 and derivates, propidium iodide33, gallamine triethiodide34 among others. In order to maintain a stable binding of these inhibitors with the enzyme, many cooperative interactions are established such as hydrogen bonds, hydrophobic contacts, π-π (aromatic) interactions, and hydrophilic-hydrophobic interactions35. The chemical structure of the evaluated compounds allows many of these interactions to be formed. For example, the free hydroxyl groups, the epoxide group and the carbonyl groups can form hydrogen bonds; the methyl groups generate nonpolar interactions and it is also feasible to form π-type interactions with the aromatic amino acids that are part of the PAS portion of the enzyme36.
Effects of aminophylline on airway epithelial-mesenchymal transition in brown Norway rats after repeated allergen challenge
Published in Experimental Lung Research, 2019
Ching-Chi Lin, Wei-Ji Chen, Shwu-Fang Liaw, Mei-Wei Lin, Shiuan-Chi Lin
Pulmonary function and acetylcholine provocation tests were conducted with the animals under general anesthesia using chloral hydrate (400 mg/kg), which was administered via intraperitoneal injection. The tests were carried out using a whole-body plethysmograph at 24 h after the final challenge, as described previously.21 These tests were done 24 h after the ovalbumin provocation test for the experimental groups and 24 h after the final saline aerosolization for the control group. The animals were then paralyzed with intravenous gallamine triethiodide (4 mg/kg) and artificially ventilated with a small animal ventilator at a tidal volume of 6 mL/kg and frequency of 60 breaths/min. All of the animals were stable without spontaneous breathing at 5 min after the gallamine injection.
Involvement of PM2.5-bound protein and metals in PM2.5-induced allergic airway inflammation in mice
Published in Inhalation Toxicology, 2018
Keiki Ogino, Kenjiro Nagaoka, Tatsuo Ito, Kei Takemoto, Tomoaki Okuda, Shoji F. Nakayama, Noriyoshi Ogino, Yuka Seki, Hiroki Hamada, Shogo Takashiba, Yoshihisa Fujikura
Bronchoconstriction was measured using the overflow method (Shibamori et al., 2006). Mice, anesthetized with pentobarbital (80 μg/kg), were connected to an artificial ventilator through a surgical incision in the trachea. A Pulmotor system was constructed with a rodent ventilator (Respirator model SN-480-7; Shinano Manufacturing Co. Ltd., Tokyo, Japan), a bronchospasm transducer (Model 7020; Ugo Basile, Comerio, Italy), and a data recorder (Omniace II data acquisition system, Model RA1300; NEC Sanei, Tokyo, Japan). Gallamine triethiodide (350 μg per mouse) was intravenously administered to inhibit spontaneous respiration, and acetylcholine was administered with stepwise increases in concentration from 62.5 to 2000 μg/kg with an interval of 1 min between each administration. Bronchoconstriction stimulated by the acetylcholine was expressed as the respiratory overflow volume as a percentage of the maximal overflow volume (100%) obtained by complete occlusion of the trachea.