Brezenoff H E, McGee J, Knight V
Acta Pharmacol Toxicol (Copenh). 1984 Oct;55(4):270-7. doi: 10.1111/j.1600-0773.1984.tb01981.x.
Intravenous injection of soman in the rat produced a rapid and dose related increase in blood pressure. The dose response curve was very steep, threshold responses occurring after intravenous injection of 10 micrograms/kg, and maximum increases of about 50 mmHg occurring after 40 micrograms/kg. Heart rate also generally increased. An increase in blood pressure also followed injection of soman subcutaneously, intramuscularly, intraperitoneally and into the cerebral ventricles, although the onset was slower and higher doses were required. The magnitude of the pressor response was correlated with the degree of AChE activity in the cortex, hypothalamus and brain stem, but not in the striatum. The pressor response was aborted or prevented by atropine, but not by methylatropine. It also was prevented by phenoxybenzamine. Atropine increased survival following an LD50 dose of soman; phenoxybenzamine prevented the pressor response but did not alter the survival rate.
给大鼠静脉注射梭曼后,血压迅速升高且与剂量相关。剂量反应曲线非常陡峭,静脉注射10微克/千克后出现阈反应,40微克/千克后血压最大升高约50毫米汞柱。心率通常也会增加。皮下、肌肉内、腹腔内和脑室内注射梭曼后血压也会升高,尽管起效较慢且需要更高剂量。升压反应的幅度与皮质、下丘脑和脑干中的乙酰胆碱酯酶(AChE)活性程度相关,但与纹状体中的AChE活性程度无关。阿托品可消除或预防升压反应,但甲基阿托品不能。苯氧苄胺也可预防升压反应。阿托品可提高梭曼半数致死剂量后的生存率;苯氧苄胺可预防升压反应,但不改变生存率。