Vandertop W P, de Vries W B, Notermans N C, Tulleken C A, Gispen W H
Department of Neurosurgery, University Hospital, Utrecht, The Netherlands.
J Auton Nerv Syst. 1995 Oct 5;55(1-2):112-4. doi: 10.1016/0165-1838(95)00034-u.
Using an animal model where the pupil diameter of the eye in anaesthetized and dark-adapted rats serves as a parameter of autonomic function, we studied the functional recovery of the parasympathetic nerve fibres in the oculomotor nerve after a crush lesion in rats with streptozotocin-induced diabetes compared with normal controls. Prior to the crush lesion, diabetic rats develop significantly (P < 0.001) smaller pupils compared with controls, and this occurs early in the course of the diabetes mellitus. As the difference in pupil diameter between control and diabetic rats persists immediately after the crush lesion, when the nervous control of the pupil is entirely due to sympathetic nerves, we suggest that the reduction in pupil diameter is due to a sympathetic neuropathy. Furthermore, we show that the functional recovery of the parasympathetic input to the iris after a crush lesion of the oculomotor nerve is not as good in diabetic rats as it is in normal control rats.
利用一种动物模型,在该模型中,麻醉且暗适应大鼠眼睛的瞳孔直径作为自主神经功能的一个参数,我们研究了链脲佐菌素诱导糖尿病大鼠动眼神经挤压损伤后动眼神经中副交感神经纤维的功能恢复情况,并与正常对照组进行了比较。在挤压损伤前,与对照组相比,糖尿病大鼠的瞳孔明显更小(P < 0.001),且这种情况在糖尿病病程早期就会出现。由于在挤压损伤后即刻,对照组和糖尿病大鼠之间的瞳孔直径差异仍然存在,此时瞳孔的神经控制完全由交感神经负责,我们认为瞳孔直径减小是由于交感神经病变所致。此外,我们还表明,动眼神经挤压损伤后,糖尿病大鼠虹膜副交感神经输入的功能恢复不如正常对照大鼠。