Gabelt B T, Robinson J C, Gange S J, Kaufman P L
Department of Ophthalmology, University of Wisconsin Medical School, Madison, USA.
Exp Eye Res. 1995 May;60(5):575-84. doi: 10.1016/s0014-4835(05)80072-7.
The role of sympathetic innervation in regulating the responses of aqueous humor flow, outflow facility and pupillary diameter to timolol and epinephrine was investigated in cynomolgus monkeys following unilateral superior cervical ganglionectomy. Aqueous humor flow was measured fluorophotometrically under pentobarbital anesthesia before the first and after the ninth of twice-daily topical doses of epinephrine, and under ketamine anesthesia before the first and after the ninth of twice-daily topical doses of timolol, 4-19 months after denervation. Baseline aqueous humor flow rates determined 2-4 months following denervation were 40% greater under ketamine than under pentobarbital anesthesia, with no difference between denervated and control eyes. Epinephrine increased aqueous humor flow by up to 50% in a dose-dependent fashion in both eyes, with a non-significant tendency toward slightly greater potency and efficacy in the denervated eyes. Timolol decreased aqueous humor flow by up to 50% in a dose-dependent fashion with equal maximal efficacy in both eyes, but with slightly and statistically significantly greater potency and efficacy in the control eyes at submaximal doses. Early (1-3 months) but not late (23-27 months) after denervation, baseline pupil diameter under ketamine anesthesia was smaller in the denervated eyes than in the controls. The mydriatic response to 600 micrograms epinephrine was more sensitive in the denervated than the control eye both early (1-3 months) and later on (23-27 months) after denervation; timolol had no effect on pupil diameter in either eye. No striking differences in intraocular pressure or refraction were observed between the eyes under any of these conditions. Resting outflow facility or resistance and perfusion-induced facility increase or resistance reduction, measured by two-level constant pressure perfusion under pentobarbital anesthesia 1.5-4.5 years after unilateral sympathectomy, did not differ significantly between sympathectomized and control eyes. Facility increased (by up to 30-50% beyond washout) and resistance decreased (by up to 20-30% beyond washout) similarly in control and sympathectomized eyes 10-60 min and 3-4 hr after bolus intracameral epinephrine doses of 0.55 and 5.5 micrograms.
在单侧颈上神经节切除后的食蟹猴中，研究了交感神经支配在调节房水生成、房水流出易度以及瞳孔直径对噻吗洛尔和肾上腺素反应中的作用。在去神经支配后4 - 19个月，于每日两次局部应用肾上腺素前及第九次用药后，在戊巴比妥麻醉下用荧光光度法测量房水生成；于每日两次局部应用噻吗洛尔前及第九次用药后，在氯胺酮麻醉下测量房水生成。去神经支配后2 - 4个月测定的基础房水生成率，在氯胺酮麻醉下比在戊巴比妥麻醉下高40%，去神经支配眼与对照眼之间无差异。肾上腺素使双眼房水生成增加高达50%，呈剂量依赖性，去神经支配眼的效力和效果略高，但无显著差异。噻吗洛尔使双眼房水生成减少高达50%，呈剂量依赖性，双眼最大效力相同，但在亚最大剂量时，对照眼的效力和效果略高且具有统计学显著差异。去神经支配后早期（1 - 3个月）而非晚期（23 - 27个月），氯胺酮麻醉下的去神经支配眼的基础瞳孔直径小于对照眼。去神经支配后早期（1 - 3个月）及后期（23 - 27个月），去神经支配眼对600微克肾上腺素的散瞳反应比对照眼更敏感；噻吗洛尔对双眼瞳孔直径均无影响。在任何这些情况下，双眼之间未观察到眼压或屈光度有明显差异。在单侧交感神经切除术后1.5 - 4.5年，于戊巴比妥麻醉下通过两级恒压灌注测量静息流出易度或阻力以及灌注诱导的流出易度增加或阻力降低，交感神经切除眼与对照眼之间无显著差异。在眼内注射0.55微克和5.5微克肾上腺素推注后10 - 60分钟及3 - 4小时，对照眼和交感神经切除眼的流出易度增加（比冲洗后高30 - 50%）和阻力降低（比冲洗后高20 - 30%）情况相似。
