Ganendran A, Balabaskaran S
Southeast Asian J Trop Med Public Health. 1976 Sep;7(3):417-23.
There is biochemical and clinical evidence that P-2-AM (Pyridine-2-Aldoxime Methiodide, Pralidoxime) does not reactive human acetylcholinesterase inhibited by either Malathion or Malaoxon. In vitro studies using Pralidoxime iodide up to ten times the recommended concentrations, produced insignificant reactivation of cholinesterases inhibited by Malathion or Malaoxon. This was observed inspite of prolonged exposure of the inhibited cholinesterases to the oxime. The value of Pralidoxime as a reactivator of phosphorylated cholinesterases is therefore in doubt, and should not be used in preference to large doses of atropine and other supportive treatment in poisoning by organophosphate pesticides.
有生化和临床证据表明，2 - 肟基吡啶（碘解磷定，派姆）不能使被马拉硫磷或马拉氧磷抑制的人乙酰胆碱酯酶重新活化。使用高达推荐浓度10倍的碘解磷定进行的体外研究表明，被马拉硫磷或马拉氧磷抑制的胆碱酯酶重新活化程度不显著。尽管被抑制的胆碱酯酶与肟长时间接触，但仍观察到上述结果。因此，碘解磷定作为磷酸化胆碱酯酶重新活化剂的价值值得怀疑，在有机磷农药中毒时，不应优先于大剂量阿托品及其他支持性治疗使用。
