Andersson S E
Department of Physiology and Medical Biophysics, University of Uppsala, Sweden.
Acta Physiol Scand. 1987 Nov;131(3):371-6. doi: 10.1111/j.1748-1716.1987.tb08252.x.
In the rat eye, intracameral injections of substance P in doses of 10-30 pmol caused a maximal long-lasting miosis and a leakage of plasma proteins into the aqueous humor, indicating a breakdown of the blood-aqueous barrier. Neurokinin A seemed equipotent to SP, but calcitonin-gene-related peptide (CGRP) (17 pmol) caused neither miosis nor protein leakage into the aqueous humor. The same result was obtained when CGRP was administered intravenously. Intracameral injection of capsaicin caused only a transient miosis which could not be repeated with further injections, even though the pupillary sphincter was still able to react to exogenous SP. Antidromic electrical stimulation of the trigeminal nerve caused plasma extravasation in the skin and a breakdown of the blood-aqueous barrier with an increased protein content in the aqueous humor. The stimulation did not affect the pupil size. The results indicate that in rat eyes SP and NKA are miotics, but the amounts that can be released from sensory nerve endings are too small to cause persistent miosis. These peptides are more likely to play a role in the neurogenic breakdown of the blood-aqueous barrier. CGRP at the same dose affects neither the pupillary sphincter muscle nor the barrier.
在大鼠眼中，前房内注射剂量为10 - 30皮摩尔的P物质会引起最大程度的持久瞳孔缩小以及血浆蛋白渗漏到房水中，这表明血-房水屏障遭到破坏。神经激肽A似乎与P物质具有同等效力，但降钙素基因相关肽（CGRP）（17皮摩尔）既不会引起瞳孔缩小，也不会导致血浆蛋白渗漏到房水中。静脉注射CGRP时也得到了相同的结果。前房内注射辣椒素仅引起短暂的瞳孔缩小，后续再次注射时无法重复这一现象，尽管瞳孔括约肌仍能对外源性P物质产生反应。三叉神经的逆向电刺激会导致皮肤出现血浆外渗以及血-房水屏障遭到破坏，房水中蛋白质含量增加。该刺激并未影响瞳孔大小。结果表明，在大鼠眼中，P物质和神经激肽A是缩瞳剂，但感觉神经末梢释放的量太小，无法引起持续性瞳孔缩小。这些肽更有可能在血-房水屏障的神经源性破坏中发挥作用。相同剂量的CGRP对瞳孔括约肌和屏障均无影响。
