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【medical-news】前列腺素降低眼内压的机制
Bahler CK, Howell KG, Hann CR, Fautsch MP, Johnson DH
Am J Ophthalmol. 2008;145:114-119
Summary
This laboratory study used perfusion of cultured human anterior segments. All eyes were enucleated within 4 hours of the time of death, and no eyes had a history of glaucoma. One anterior segment was perfused with a continuous amount of drug and the fellow anterior chamber was monitored without drug. Histologic changes and assessment of MMP activity was then performed. This model was partly chosen because it eliminates the role of the uveoscleral pathway because of absence of the choroid and a functioning ciliary body.
Latanoprost increased outflow facility (an increase of 67%), with changes occurring within 1 hour of receiving drug, whereas PGE caused less of a change in outflow (an increase of 13%) facility. These changes were reversible after the drugs were removed. Histopathologic specimens showed focal detachment and loss of endothelial cells within the canal of Schlemm. There was no consistent pattern of MMP activity. Although scleral hydraulic conductivity increased, the change was not enough to account for the entire change in outflow facility.
Comment
Based on 2 main lines of evidence, the authors suggested that a pressure-sensitive mechanism for the outflow of aqueous humor is important. First, they pointed to an absence of changes in MMPs in the trabecular meshwork. If changes in the trabecular meshwork were solely responsible for the decreases in IOP seen with prostaglandins, then changes in MMP activity would be expected. The second piece of evidence was based on fluid flow through the sclera. Because scleral outflow was measured to be lower than the outflow facility, trabecular outflow appears to be increased by prostaglandins. The authors suggest that because of this mechanism, future drug and gene therapy targets in glaucoma might be influenced.
http://www.medscape.com/viewarticle/571410 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领 Summary
This laboratory study used perfusion of cultured human anterior segments.
这项实验研究对培养过的人眼前房进行灌注。
All eyes were enucleated within 4 hours of the time of death, and no eyes had a history of glaucoma.
所有的眼球都是在主人死亡的4个小时内被剜出并且都没有青光眼病史。
One anterior segment was perfused with a continuous amount of drug and the fellow anterior chamber was monitored without drug.
一组对眼前段连续灌注相当数量的药物，而另一组不给药而予以监测。
Histologic changes and assessment of MMP activity was then performed.
（实验组的眼组织）组织学特征发生了改变，接下来对间质金属蛋白酶活性进行评价。
This model was partly chosen because it eliminates the role of the uveoscleral pathway because of absence of the choroid and a functioning ciliary body.因为缺乏脉络膜和功能性的睫状体，该模型忽略了葡萄膜巩膜旁路小路的作用因而只具有部分可靠性。
Latanoprost increased outflow facility (an increase of 67%), with changes occurring within 1 hour of receiving drug, whereas PGE caused less of a change in outflow (an increase of 13%) facility.
拉坦前列腺素增加了房水流畅度(67%)，在给药1个小时内发生变化。而前列腺素E增加的房水流畅度较其少(13%)。
These changes were reversible after the drugs were removed.
在停止给药后，房水流畅度的变化是可逆的。
Histopathologic specimens showed focal detachment and loss of endothelial cells within the canal of Schlemm.
组织病理检查发现在Schlemn管内有内皮细胞的局部脱落和丢失。
There was no consistent pattern of MMP activity.
没有发现间质金属蛋白持续保持活性。
Although scleral hydraulic conductivity increased, the change was not enough to account for the entire change in outflow facility.
尽管房水通过巩膜外流的能力有提高，但并不足以解释外流结构的整体变化。
Comment
Based on 2 main lines of evidence, the authors suggested that a pressure-sensitive mechanism for the outflow of aqueous humor is important.
基于证据的2条主线，作者认为一个房水外流的压力敏感机制发挥了重要作用。
First, they pointed to an absence of changes in MMPs in the trabecular meshwork.
首先，在小梁网上缺少间质金属蛋白含量上的变化。
If changes in the trabecular meshwork were solely responsible for the decreases in IOP seen with prostaglandins, then changes in MMP activity would be expected.
如果眼内压的下降仅因为前列腺素含量在小梁网里的变化，则间质金属蛋白的活性改变也将发现。
The second piece of evidence was based on fluid flow through the sclera.
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作者:admin@医学,生命科学 2010-10-29 17:11
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