de Neef J H, Manneke A, Porsius A J
Arch Toxicol. 1982 Sep;50(3-4):241-7. doi: 10.1007/BF00310856.
In the present study paraoxon (28-825 micrograms/kg, i.v.) was administered into rabbits treated with N-methylatropine (1 mg/kg). In urethane-anaesthetized rabbits pressor and depressor effects were observed. In pentobarbitone-anaesthetized rabbits, however, only depresssor effects were noticed. Dexetimide (0.25-0.5 mg/kg) prevented the pressor and depressor action of paraoxon. Furthermore, paraoxon (83-825 micrograms) was infused into a vertebral artery of pentobarbitone-anaesthetized animals. After administration via this route the depressor effect was similar to i.v. administration. 30 min after administration of paraoxon acetylcholinesterase activity was determined in the medulla oblongata, the pons and the hypothalamus. The enzyme has to be inhibited almost completely to induce an effect on blood pressure. It is concluded that the vascular effects of paraoxon seem to be mediated by a mechanism involving stimulation of central muscarinic receptors, probably by accumulated acetylcholine, which in turn induces a decrease in blood pressure.
在本研究中,对用N - 甲基阿托品(1毫克/千克)处理过的家兔静脉注射对氧磷(28 - 825微克/千克)。在氨基甲酸乙酯麻醉的家兔中观察到升压和降压作用。然而,在戊巴比妥麻醉的家兔中,仅观察到降压作用。地昔替明(0.25 - 0.5毫克/千克)可防止对氧磷的升压和降压作用。此外,将对氧磷(83 - 825微克)注入戊巴比妥麻醉动物的椎动脉。通过该途径给药后,降压作用与静脉注射相似。对氧磷给药30分钟后,测定延髓、脑桥和下丘脑的乙酰胆碱酯酶活性。必须几乎完全抑制该酶才能对血压产生影响。得出的结论是,对氧磷的血管效应似乎是由一种机制介导的,该机制涉及刺激中枢毒蕈碱受体,可能是由积累的乙酰胆碱介导,进而导致血压下降。