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在地氟烷麻醉期间,交感神经系统并不介导反射性瞳孔扩张。

Sympathetic nervous system does not mediate reflex pupillary dilation during desflurane anesthesia.

作者信息

Larson M D, Tayefeh F, Sessler D I, Daniel M, Noorani M

机构信息

Department of Anesthesia, University of California, San Francisco 94143-0648, USA.

出版信息

Anesthesiology. 1996 Oct;85(4):748-54. doi: 10.1097/00000542-199610000-00009.

Abstract

BACKGROUND

Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system. Noxious stimulation dilates the pupil in both unanesthetized and anesthetized humans. In the absence of anesthesia, dilation is primarily mediated by the sympathetic nervous system. In contrast, pupillary dilation in cats given barbiturate or cloralose anesthesia is mediated solely by inhibition of the midbrain parasympathetic nucleus. The mechanism by which noxious stimuli dilate pupils during anesthesia in humans remains unknown. Accordingly, the authors tested the hypothesis that the pupillary dilation in response to noxious stimulation during desflurane anesthesia is primarily a parasympathetic reflex.

METHODS

In six volunteers, the alpha-I adrenergic receptors of the iris musculature were blocked by unilateral administration of topical dapiprazole; six other volunteers were given unilateral topical tropicamide to block the muscarinic receptors in the iris. Desflurane anesthesia was subsequently induced in all volunteers. Sympathetic nervous system activation, with reflex dilation of the pupil, was produced by noxious electrical stimulation during 4% and 8% end-tidal desflurane, and by a rapid 4%-to-8% step-up in the desflurane concentration. Pupil diameter and the change in pupil size induced by a light stimulus (light reflex amplitude) were measured with infrared pupillometry.

RESULTS

Dapiprazole drops produced a Horner's miosis, but pupils were equally small after induction of anesthesia. Pupillary dilation after noxious stimulation and desflurane step-up was identical in the unblocked and dapiprazole-blocked pupils. After tropicamide administration, the pupil was dilated and the light reflex was completely inhibited. Noxious stimulation nonetheless produced a slight additional dilation.

CONCLUSIONS

During desflurane anesthesia, pupillary dilation in response to noxious stimulation or desflurane step-up is not mediated by the sympathetic nervous system (as it is in unanesthetized persons). Although inhibition of the pupillo-constrictor nucleus may be the cause of this dilation, the mechanism remains unknown.

摘要

背景

瞳孔大小由自主神经系统的交感神经和副交感神经分支之间的相互作用决定。有害刺激会使未麻醉和麻醉状态下的人的瞳孔扩大。在无麻醉状态下,瞳孔扩大主要由交感神经系统介导。相比之下,给予巴比妥酸盐或氯醛糖麻醉的猫的瞳孔扩大仅由中脑副交感神经核的抑制介导。在人类麻醉期间,有害刺激使瞳孔扩大的机制尚不清楚。因此,作者检验了以下假设:在地氟醚麻醉期间,对有害刺激的瞳孔扩大主要是一种副交感神经反射。

方法

在6名志愿者中,通过单侧局部应用达哌唑阻断虹膜肌肉组织的α-1肾上腺素能受体;另外6名志愿者单侧局部应用托吡卡胺以阻断虹膜中的毒蕈碱受体。随后所有志愿者均接受地氟醚麻醉。在呼气末地氟醚浓度为4%和8%期间,通过有害电刺激以及地氟醚浓度从4%快速升至8%来激活交感神经系统并使瞳孔反射性扩大。用红外瞳孔测量法测量瞳孔直径和光刺激引起的瞳孔大小变化(光反射幅度)。

结果

滴入达哌唑产生霍纳氏瞳孔缩小,但麻醉诱导后瞳孔同样变小。在未阻断和达哌唑阻断的瞳孔中,有害刺激和地氟醚浓度升高后的瞳孔扩大情况相同。应用托吡卡胺后,瞳孔扩大且光反射完全被抑制。然而,有害刺激仍会导致轻微的额外扩大。

结论

在地氟醚麻醉期间,对有害刺激或地氟醚浓度升高的瞳孔扩大并非由交感神经系统介导(与未麻醉者的情况相同)。尽管瞳孔收缩核的抑制可能是这种扩大的原因,但其机制仍然未知。

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