Aas P
Norwegian Defence Research Establishment, Division for Environmental Toxicology, Kjeller, Norway.
Toxicology. 1988 Apr;49(1):91-7. doi: 10.1016/0300-483x(88)90179-5.
Excessive cholinergic stimulation of presynaptic muscarinic cholinergic receptors, due to complete inhibition of acetylcholinesterase (AChE) by O-(1,2,2-trimethylpropyl)-methyl-phosphonofluoridate (soman), reduced the release of acetylcholine (ACh) from cholinergic nerves in rat bronchi by almost 25%. Furthermore, long-term (40 h) exposure by inhalation of soman (0.45-0.63 mg/m3) reduced the contraction of bronchi induced by ACh by approximately 70%. This is probably due to reduction of the number of muscarinic cholinergic receptors, since there was a reduction in the binding capacity (Bmax) of [3H]QNB by 40%, without any changes in the dissociation constant (Kd).
O-（1,2,2-三甲基丙基）-甲基磷酰氟（梭曼）对乙酰胆碱酯酶（AChE）的完全抑制作用导致突触前毒蕈碱型胆碱能受体的胆碱能刺激过度，使大鼠支气管中胆碱能神经释放的乙酰胆碱（ACh）减少了近25%。此外，长期（40小时）吸入梭曼（0.45 - 0.63毫克/立方米）使ACh诱导的支气管收缩减少了约70%。这可能是由于毒蕈碱型胆碱能受体数量减少，因为[3H]QNB的结合容量（Bmax）降低了40%，而解离常数（Kd）没有任何变化。
