Bartels S P, Pawlowski A M
Ophthalmic Pharmacology Unit, Eye Research Institute of Retina Foundation, Boston, MA.
Curr Eye Res. 1990 Oct;9(10):927-34. doi: 10.3109/02713689009069929.
The effect of electrical stimulation of the sympathetic nerves on the blood-aqueous barrier was investigated in rabbits. The permeability of the barrier was assessed during either acute, chronic or following chronic nerve stimulation. During acute and chronic stimulation of the sympathetic nerves, fluorescein entered the anterior chamber at a rate significantly slower than in control eyes. After chronic stimulation, both the rate of entry of fluorescein and the aqueous humor protein concentration were much greater than in control eyes indicating breakdown of the blood-aqueous barrier. Treatment with the non-steroidal anti-inflammatory drugs, indomethacin and suprofen, completely blocked the breakdown of the blood-aqueous barrier. These results indicate that sympathetic nerve stimulation can cause the local synthesis of prostaglandins and that these can affect the blood-aqueous barrier.
在兔身上研究了交感神经电刺激对血-房水屏障的影响。在急性、慢性或慢性神经刺激后评估该屏障的通透性。在交感神经急性和慢性刺激期间,荧光素进入前房的速率明显慢于对照眼。慢性刺激后,荧光素的进入速率和房水蛋白浓度均远高于对照眼,表明血-房水屏障被破坏。用非甾体抗炎药吲哚美辛和舒洛芬治疗可完全阻止血-房水屏障的破坏。这些结果表明,交感神经刺激可引起前列腺素的局部合成,且这些前列腺素可影响血-房水屏障。