Alessandri M, Pietrini U, Bandini E B, Beatrice S, Fanciullacci M
Institute of Internal Medicine and Therapeutics IV, Headache Centre, Florence University, Italy.
Clin Neuropharmacol. 1992 Apr;15(2):120-8. doi: 10.1097/00002826-199204000-00006.
In 12 healthy volunteers, the effects of a single oral dose of nimodipine (40 mg) on pupil size and on the mydriasis induced by conjunctival instillation of tyramine and phenylephrine were studied by using a TV monocular infrared pupillometer. Nimodipine alone was unable to modify the pupil area. When compared with placebo, the Ca2+ entry blocker reduced the pupil dilation caused by tyramine, whereas it did not affect the phenylephrine-induced mydriasis. Since tyramine provokes mydriasis by releasing neuronal norepinephrine, a full adrenoceptor agonist, whereas phenylephrine acts only on alpha 1-adrenoceptors insensitive of extracellular Ca2+, the hypothesis may be advanced that a heterogeneous population of alpha-adrenoceptors, located in the human iris dilator muscle and differently sensitive to Ca2+ entry blockade, is responsible for the reduction of the tyramine-induced mydriasis. Apart from this putative mechanism, the results suggest that nimodipine reduces the pupillary response to adrenergic activation in the human eye.
在12名健康志愿者中，使用电视单目红外瞳孔计研究了单次口服尼莫地平（40毫克）对瞳孔大小以及由结膜滴注酪胺和去氧肾上腺素引起的散瞳的影响。单独使用尼莫地平无法改变瞳孔面积。与安慰剂相比，钙通道阻滞剂减少了酪胺引起的瞳孔扩张，而对去氧肾上腺素引起的散瞳没有影响。由于酪胺通过释放神经元去甲肾上腺素（一种完全的肾上腺素能受体激动剂）引起散瞳，而去氧肾上腺素仅作用于对细胞外钙不敏感的α1-肾上腺素能受体，因此可以提出这样的假设，即位于人虹膜开大肌中且对钙通道阻滞敏感性不同的异质性α-肾上腺素能受体群体，是酪胺引起的散瞳减弱的原因。除了这种推测的机制外，结果表明尼莫地平降低了人眼中对肾上腺素能激活的瞳孔反应。
