Korczyn A D, Keren O, Eshel Y
Isr J Med Sci. 1982 Jan;18(1):145-7.
Amantadine, injected into mice, produces dose-dependent mydriasis. The pupillary dilation caused by amantadine is not abolished by pretreatment with reserpine, or by combined pretreatment with reserpine and alpha-methyl-p-tyrosine, although the mydriasis is reduced by approximately 25%. Thus, release of catecholamines from nerve terminals can account for only 25% of amantadine-produced mydriasis. Haloperidol and phentolamine can partially block the effect of amantadine, but, when given after reserpine, neither of the antagonists increases the blockade produced by reserpine alone. We conclude that the catecholaminergic system contributes only partially to the pupillary effect of amantadine, and that other mechanisms appear to be involved.
将金刚烷胺注射到小鼠体内会产生剂量依赖性瞳孔散大。尽管用利血平预处理或用利血平和α-甲基对酪氨酸联合预处理可使金刚烷胺引起的瞳孔散大减少约25%,但这种瞳孔散大并未被消除。因此,神经末梢释放的儿茶酚胺仅占金刚烷胺所致瞳孔散大的25%。氟哌啶醇和酚妥拉明可部分阻断金刚烷胺的作用,但在利血平给药后给予这两种拮抗剂,均不会增强利血平单独产生的阻断作用。我们得出结论,儿茶酚胺能系统仅部分参与了金刚烷胺的瞳孔效应,似乎还涉及其他机制。