Miyake K, Shirasawa E, Hikita M, Miyake Y, Kuratomi R
Shohzankai Medical Foundation, Miyake Eye Hospital, Nagoya, Japan.
Invest Ophthalmol Vis Sci. 1988 Feb;29(2):332-4.
Using radioimmunoassay techniques, we measured the amounts of prostaglandin E (PGE) in the aqueous humor and vitreous body of 22 phakic and ten aphakic rabbit eyes. Either epinephrine and placebo, epinephrine and indomethacin, indomethacin and placebo, or placebo and placebo were administered topically for 5 months. Treatment of aphakic eyes was initiated 1 month after intracapsular lens extraction. Topically applied epinephrine apparently induced the synthesis of prostaglandin, manifested by elevated PGE in the aqueous and vitreous. Phakic eyes treated with epinephrine and placebo had mean PGE levels of 407.33 pg/ml in the aqueous and 177.0 pg/ml in the vitreous, whereas control eyes given only placebo had mean levels of 165.83 in aqueous and 59.17 in vitreous. Topically applied indomethacin inhibited epinephrine-induced synthesis of PGE in the aqueous humor, but had no significant effect in the vitreous. PGE levels, higher in placebo-treated aphakic eyes than in phakic ones, were elevated further by epinephrine treatment (from 388.40 to 1851.60 pg/ml in aqueous of aphakic eyes, and from 236.40 to 850.60 pg/ml in vitreous also of aphakic eyes). Our findings relate to the pathogenesis of epinephrine-induced maculopathy and to the mechanism of the ocular hypotensive effect of epinephrine.
我们运用放射免疫分析技术,测定了22只透明晶体眼和10只无晶体眼兔眼房水和玻璃体中前列腺素E(PGE)的含量。局部应用肾上腺素和安慰剂、肾上腺素和吲哚美辛、吲哚美辛和安慰剂,或安慰剂和安慰剂,持续5个月。在囊内晶状体摘除术后1个月开始对无晶体眼进行治疗。局部应用肾上腺素显然诱导了前列腺素的合成,表现为房水和玻璃体中PGE升高。用肾上腺素和安慰剂治疗的透明晶体眼房水中PGE平均水平为407.33 pg/ml,玻璃体中为177.0 pg/ml,而仅给予安慰剂的对照眼房水和玻璃体中的平均水平分别为165.83和59.17。局部应用吲哚美辛抑制了肾上腺素诱导的房水中PGE的合成,但在玻璃体中无显著作用。安慰剂治疗的无晶体眼的PGE水平高于透明晶体眼,肾上腺素治疗使其进一步升高(无晶体眼房水从388.40 pg/ml升至1851.60 pg/ml,玻璃体也从236.40 pg/ml升至850.60 pg/ml)。我们的研究结果与肾上腺素诱导的黄斑病变的发病机制以及肾上腺素的眼压降低作用机制有关。