(19) Inhibition of guinea pig hemi-diaphragm acetylcholinesterase activity by pyridostigmine bromide and protection against soman toxicity

2005 ◽  
Vol 157-158 ◽  
pp. 381-382 ◽  
Author(s):  
Julian R. Haigh ◽  
Scott R. Johnston ◽  
Brian M. Peters ◽  
Bhupendra P. Doctor ◽  
Richard K. Gordon ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Acetylcholinesterase Activity ◽  
Pyridostigmine Bromide

The Effect of Continuous Pyridostigmine Administration on Functional (A12) Acetylcholinesterase Activity in Guinea-Pig Muscles

2001 ◽  
Vol 22 (6) ◽  
pp. 787-793 ◽  
Author(s):  
Maxine C. Lintern ◽  
Janet R. Wetherell ◽  
Christopher Taylor ◽  
Margaret E. Smith
Keyword(s):  
Guinea Pig ◽  
Acetylcholinesterase Activity

Protection by pyridostigmine bromide of marmoset hemi-diaphragm acetylcholinesterase activity after soman exposure

2010 ◽  
Vol 187 (1-3) ◽  
pp. 416-420 ◽  
Author(s):  
Julian R. Haigh ◽  
Michael Adler ◽  
James P. Apland ◽  
Sharad S. Deshpande ◽  
Charles B. Barham ◽  
...  
Keyword(s):  
Acetylcholinesterase Activity ◽  
Pyridostigmine Bromide

Differences between inhaled and intravenous bronchial challenge to detect O3-induced hyperresponsiveness

2001 ◽  
Vol 91 (6) ◽  
pp. 2595-2601 ◽  
Author(s):  
Bettina Sommer ◽  
Mario H. Vargas ◽  
Jaime Chavez ◽  
Veronica Carbajal ◽  
Patricia Segura ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Airway Hyperresponsiveness ◽  
Acetylcholinesterase Activity ◽  
Laboratory Animals ◽  
Response Curves ◽  
Air Exposure ◽  
Blood Samples ◽  
Mechanically Ventilated ◽  
Administration Routes ◽  
Spontaneously Breathing

Ozone (O3)-induced airway hyperresponsiveness in laboratory animals is usually demonstrated through dose-response curves with inhaled or intravenous bronchoconstrictor agonists. However, comparability of these two routes has not been well documented. Thus guinea pig airway responsiveness to ACh and histamine was evaluated 16–18 h after O3 (3 parts/million, 1 h) or air exposure by two plethysmographic methods (spontaneously breathing and mechanically ventilated) and by two administration routes (inhalatory or intravenous). We found that O3 caused airway hyperresponsiveness to intravenous, but not to inhaled, agonists, independent of the plethysmographic method used. Suitability of the inhalatory route to detect airway hyperresponsiveness was corroborated with inhaled ACh after an antigen challenge or extending O3exposure to 3 h. Acetylcholinesterase activity was not modified after O3 exposure in lung homogenates and blood samples. Thus inhaled agonists were less effective to reveal the airway hyperresponsiveness after an acute O3 exposure than intravenous ones, at least for the 1-h exposure to 3 parts/million, and this difference seems not to be related to an O3-induced inhibition of the acetylcholinesterase activity.

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