Effects of Ocular Hypotensive Agents on Prostaglandin-Mediated Elevation of Intraocular Pressure
Effects of Ocular Hypotensive Agents on Prostaglandin-Mediated Elevation of Intraocular Pressure
复制标题
降眼压药对前列腺素介导的眼压升高的影响
DOI：
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发表时间：
1978
期刊：
影响因子：
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通讯作者：
P. Vareilles
中科院分区：
文献类型：
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作者：
P. Conquet;P. Vareilles
明显的血管舒张伴随着血水屏障的破裂是解释前列腺素（pg）或其前体引起的眼压（IOP）升高的最具文献依据的假说。然而，不排除对纤毛过程分泌机制的直接作用。为了探索后一种可能性，我们在家兔身上测试了能够通过不同机制降低IOP的化合物对花生四烯酸（AA）和PGE2诱导的实验性IOP升高的影响。局部给药50 μ1 0.5% AA或0.01% PGE2溶液作为标准眼压剂量。观察肾上腺素、去甲肾上腺素、苯肾上腺素和异丙肾上腺素外用和乙酰唑胺口服对AA和PGE2 IOP反应的影响。分别在给药后30min和4h观察AA的IOP升高情况。PGE2只使用一个实验时间（30min）来确认AA获得的数据。30min时，α-和混合αβ-肾上腺素激动剂以剂量相关的方式抑制pg介导的IOP升高。相反，在降压效果最大的4小时时，它们对这些反应没有影响。β-肾上腺素能激动剂和乙酰唑胺在两个实验时间均不影响AA或PG的反应。肾上腺素、去甲肾上腺素和苯肾上腺素的抑制作用归因于它们的血管收缩特性，而不是对房水分泌机制的影响。这些结果反驳了pg通过直接作用于分泌机制而提高IOP的既定假设，并为pg对眼睛的血管作用提供了额外的证据。
Marked vasodilation followed by a rupture of the blood aqueous barrier is the best-documented hypothesis to explain the rise of intraocular pressure (IOP) induced by prostaglandins (PGs) or their precursors. However, a direct action on secretory mechanisms in the ciliary processes may not be excluded. To explore the latter possibility, compounds capable of decreasing IOP by different mechanisms have been tested in rabbits for their effects on experimentally elevated IOP induced by arachidonic acid (AA) and PGE2. Topical administration of 50 μ1of 0.5% AA or 0.01% PGE2 solutions was utilized as standard ocular hypertensive doses. Epinephrine, norepinephrine, phenylephrine and isoproterenol administered topically and acetazolamide administered orally were tested for their effects on the IOP response to AA and PGE2. The IOP elevation due to AA instillation was studied at 30 min and 4 h after administration of the test agents. Only one experimental time (30 min) was used for PGE2 to confirm the data obtained with AA. At 30 min, α- and mixed αβ-adrenerig agonists inhibited in a dose-related manner the PG-mediated elevation of IOP. In contrast, they did not affect these reactions at 4 h when their ocular hypotensive effect was maximal. The β-adrenergic agonist and acetazolamide did not influence AA or PG responses at either experimental time. The inhibition observed with epinephrine, norepinephrine and phenylephrine was attributed to their vasoconstrictive properties rather than to an effect on aqueous humor secretory mechanisms. These results argue against the formulated hypothesis that PGs elevate IOP by a direct action on secretory mechanism and give additional evidence for a vascular effect of PGs on the eye.