Malave A, Holsapple M P, Yim G K
Life Sci. 1982 Mar 15;30(11):929-34. doi: 10.1016/0024-3205(82)90621-x.
The aim of this study was to assess the possible role of a central cholinergic component phencyclidine (PCP)-induced hypertension. Sprague-Dawley rats, lightly anesthetized with urethane, exhibited a dose related pressor response following 0.1-1.0 mg/kg PCP i.v. After i.v. atropine pretreatment, the PCP dose-response curve was shifted to the right, and the magnitude of the pressor responses was reduced by about 50%. In addition, atropine reduced the incidence of apneusis, but had no effect on the bradycardia that accompanied the pressor responses. Methylatropine (i.v.) did not reduce the PCP pressor responses, nor did it prevent the apneusis induced by PCP. These results suggest that in addition to its direct pressor effects the activation of central cholinergic systems contribute significantly to the cardiovascular and respiratory toxicity induced by PCP.
本研究的目的是评估中枢胆碱能成分在苯环利定(PCP)诱导的高血压中可能发挥的作用。用乌拉坦轻度麻醉的Sprague-Dawley大鼠,静脉注射0.1 - 1.0 mg/kg PCP后呈现出剂量相关的升压反应。静脉注射阿托品预处理后,PCP剂量-反应曲线右移,升压反应幅度降低约50%。此外,阿托品降低了呼吸暂停的发生率,但对伴随升压反应的心动过缓没有影响。甲基阿托品(静脉注射)既没有降低PCP的升压反应,也没有预防PCP诱导的呼吸暂停。这些结果表明,除了其直接的升压作用外,中枢胆碱能系统的激活对PCP诱导的心血管和呼吸毒性有显著贡献。