Accession Number : ADA254329


Title :   Autonomic Cholinergic Neurotransmission in the Respiratory System: Effect of Organophosphate Poisoning and Its Treatment


Descriptive Note : Doctoral thesis


Corporate Author : NORWEGIAN DEFENCE RESEARCH ESTABLISHMENT KJELLER


Personal Author(s) : Walday, Per


Full Text : https://apps.dtic.mil/dtic/tr/fulltext/u2/a254329.pdf


Report Date : May 1992


Pagination or Media Count : 105


Abstract : The present study has shown that the organophosphate anticholinesterase soman inhibits the acetylcholinesterase (AChE), butyrylcholinesterase (BuChE), and carboxylesterase (CarbE) activities in the respiratory system in vitro (rat and guinea pig) and in vivo after inhalation exposure (rat). The rat and guinea pig in vitro bronchial smooth muscle response, and the rat ex vivo tracheal response to nerve-mediated stimulation, were substantially inhibited by soman. This was probably due to an increased basal tone of the smooth muscle, induced by decreased inactivation and subsequent accumulation of acetylcholine (ACh) in the neuroeffector junctions. In vitro bronchial contractions induced by histamine in guinea pig were, however, not affected by soman, indicating that soman does not affect the airway smooth muscle itself but only the cholinergic system. During inhalation with soman, CarbE both in the respiratory system and plasma may function as a detoxifying scavenger. Addition of HI-6 and Toxogonin after in vitro exposure to soman reestablished the rat tracheal smooth muscle contraction when added 10 min, but not 30 min, after soman. The recovery induced.


Descriptors :   *RESPIRATORY SYSTEM , *CHOLINESTERASE INHIBITORS , *ORGANOPHOSPHATES , FUNCTIONS , RECOVERY , RATS , THESES , POISONING , MUSCLES , RESPONSE(BIOLOGY) , NORWAY , ACCUMULATION , ACETYLCHOLINESTERASE , NERVES , CONTRACTION , INACTIVATION , INHALATION , SWINE , GUINEA PIGS , HISTAMINE , ACETYLCHOLINE


Subject Categories : Medicine and Medical Research
      Chemical, Biological and Radiological Warfare


Distribution Statement : APPROVED FOR PUBLIC RELEASE