Pressman M R, DiPhillipo M A, Forst-Paulus M, Fry J M
Clin Neuropharmacol. 1986;9(5):464-8. doi: 10.1097/00002826-198610000-00007.
Recent evidence suggests that endogenous opiates may be involved in the pathophysiology of narcolepsy. To test this theory, the effect of 0.8 mg naloxone hydrochloride on pupil size and subjective alertness was measured in normal and narcoleptic subjects. Naloxone resulted in significant pupillary constriction in the normal but not in the narcoleptic subjects. The extent of contraction of the pupil light reflex was reduced significantly in the narcoleptic but not in the normal subjects. There was no effect on subjective ratings of alertness on the Stanford Sleepiness Scale or the visual analogue scale in either group. The naloxone-related miosis in the normal group confirms that naloxone is not a pure opiate antagonist. The lack of naloxone-related miosis in the narcoleptics suggests that narcoleptic individuals do not respond to naloxone as do normal individuals. However, this difference can not be definitely attributed to the antagonism of endogenous opiates. The reduction of the extent of contraction of the light reflex suggests that naloxone caused an increase in supranuclear inhibition of parasympathetic pupil reflex activity. However, this finding may have resulted from mechanical limitations of a small pupil or technical limitations of the recording equipment. This study does not support previous reports that naloxone causes an increase in subjective alertness in narcoleptics.
最近的证据表明，内源性阿片类物质可能参与发作性睡病的病理生理过程。为验证这一理论，在正常人和发作性睡病患者中测量了0.8毫克盐酸纳洛酮对瞳孔大小和主观警觉性的影响。纳洛酮使正常受试者出现明显的瞳孔收缩，但发作性睡病患者未出现。在发作性睡病患者中，瞳孔对光反射的收缩程度显著降低，而正常受试者则未出现这种情况。两组受试者在斯坦福嗜睡量表或视觉模拟量表上的主观警觉性评分均未受影响。正常组中与纳洛酮相关的瞳孔缩小证实纳洛酮并非纯粹的阿片类拮抗剂。发作性睡病患者缺乏与纳洛酮相关的瞳孔缩小表明，发作性睡病患者对纳洛酮的反应与正常人不同。然而，这种差异不能明确归因于内源性阿片类物质的拮抗作用。光反射收缩程度的降低表明，纳洛酮导致了副交感神经瞳孔反射活动的核上抑制增加。然而，这一发现可能是由于小瞳孔的机械限制或记录设备的技术限制所致。本研究不支持先前关于纳洛酮可提高发作性睡病患者主观警觉性的报道。
