Enzyme-induced posterior vitreous detachment in the rat produces increased lens nuclear pO2 levels.

Enzyme-induced posterior vitreous detachment in the rat produces increased lens nuclear pO2 levels.
复制标题

酶诱导的大鼠后玻璃体脱离会产生透镜核PO2水平的增加。

DOI:
10.1016/j.exer.2008.09.003
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发表时间:
2009-02
影响因子:
3.4
通讯作者:
Trese, M. T.
Trese, M. T.
中科院分区:
医学3区
文献类型:
--
作者:
Giblin, F. J.;Quiram, P. A.;Leverenz, V. R.;Baker, R. M.;Dang, Loan;Trese, M. T.

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有人提出,正常玻璃体液的破坏可能会使氧气更容易从视网膜移动到晶状体中心,从而导致核性白内障。在本研究中,我们将酶玻璃体内注射到豚鼠(具有无血管视网膜)和大鼠(具有血管视网膜)中,以产生玻璃体液液化加后玻璃体脱离(PVD)(使用微纤溶酶)或仅玻璃体液液化(使用透明质酸酶),并在1-2周后进行测量 使用铂基荧光团 O2 传感器(Oxford-Optronix, Ltd.)测定体内晶状体核 pO2 水平。还进行了玻璃体内注射微纤溶酶或透明质酸酶后允许动物呼吸 100% O2 的实验,以研究对眼内 O2 交换的可能影响。与对照组相比,1-2 周后,给豚鼠注射这两种酶中的任何一种,晶状体 pO2 水平没有产生显着差异。然而,与对照组相比,注射微纤溶酶的大鼠晶状体中心的 O2 水平增加了 68%(5.6 mmHg 增加至 9.4 mmHg,p<0.05),而在类似使用透明质酸酶后没有观察到相应的效果。当豚鼠随后被允许呼吸 100% O2 时,用微纤溶酶治疗的豚鼠显着加速了 O2 穿过玻璃体腔的移动(例如,O2 到达晶状体正后方的位置的速度比对照快 5 倍;p<0.01);然而,用透明质酸酶治疗后的效果明显减弱。当注射微纤溶酶的大鼠呼吸 100% O2 时,O2 到达晶状体中心所需的时间比对照组快 3 倍(0.4 分钟与 1.4 分钟相比,p<0.01)。该结果对于人类中与年龄相关的PVD的发生以及可能加速成熟期核性白内障的发生具有重要意义。此外,酶法产生PVD以增加玻璃体腔内的O2交换率可能具有治疗视网膜缺血性疾病的潜在应用。
It has been proposed that disruption of normal vitreous humor may permit O2 to travel more easily from the retina to the center of the lens where it may cause nuclear cataract. In the present study, we injected enzymes intravitreally into guinea pigs (which possess an avascular retina) and rats (which possess a vascular retina) to produce either vitreous humor liquefaction plus a posterior vitreous detachment (PVD) (with use of microplasmin) or vitreous humor liquefaction only (with use of hyaluronidase), and 1–2 weeks later measured lens nuclear pO2 levels in vivo using a platinum-based fluorophore O2 sensor (Oxford-Optronix, Ltd.). Experiments were also conducted in which the animals were allowed to breathe 100% O2 following intravitreal injection with either microplasmin or hyaluronidase in order to investigate possible effects on O2 exchange within the eye. Injection of guinea pigs with either of the two enzymes produced no significant differences in lens pO2 levels 1–2 weeks later, compared to controls. However, for the rat, injection of microplasmin produced a 68% increase in O2 level in the center of the lens, compared to the controls (5.6 mmHg increasing to 9.4 mmHg, p<0.05), with no corresponding effect observed following similar use of hyaluronidase. Treatment of guinea pigs with microplasmin dramatically accelerated movement of O2 across the vitreal space when the animals were later allowed to breathe 100% O2 (for example, O2 traveled to a location directly behind the lens 5 times faster than control; p<0.01); however, the effect following treatment with hyaluronidase was significantly less. When microplasmin-injected rats breathed 100% O2, the time required for O2 to reach the center of the lens was 3 times faster than control (0.4 min compared to 1.4 min, p<0.01). The results have implication with regard to the occurrence of age-related PVD in the human, and a possible acceleration of maturity-onset nuclear cataract. In addition, enzymatic creation of a PVD to increase the rate of O2 exchange within the vitreal space may have potential application for treatment of retinal ischemic disease.
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