Vaghefi Ehsan, Kim Andy, Donaldson Paul J
School of Optometry and Vision Science School of Medical Sciences, New Zealand National Eye Center, University of Auckland, Aukland, New Zealand 2Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
School of Optometry and Vision Science School of Medical Sciences, New Zealand National Eye Center, University of Auckland, Aukland, New Zealand.
Invest Ophthalmol Vis Sci. 2015 Nov;56(12):7195-208. doi: 10.1167/iovs.15-17861.
To determine whether the cellular physiology of the lens actively maintains the optical properties of the lens and whether inhibition of lens transport affects overall visual quality.
One lens from a pair of bovine lenses was cultured in artificial aqueous humor (AAH), while the other was cultured in either AAH-High-K+ or AAH + 0.1 mM ouabain for 4 hours. Lens pairs or whole enucleated eyes were then imaged in 4.7 Tesla (T) high-field small animal magnet. Lens surface curvatures, T1 measurements of water content, and T2 measurements of water/protein ratios were extracted from cultured lenses, while the geometrical parameters that define the optical pathway were obtained from whole eyes. Gradients of refractive index (GRIN), calculated from T2 measurements, and the extracted geometric parameters were inputted into optical models of the isolated lens and the whole bovine eye.
Inhibiting circulating fluxes by inhibiting the Na/K-ATPase with ouabain or depolarization of the lens potential by High K+ caused changes to lens water content, the water/protein ratio (GRIN) and surface geometry that manifested as an increase in optical power and a decrease in negative spherical aberration in cultured lenses. Changes to optical properties of the lens resulted in a myopic shift that impaired vision quality in the optical model of the bovine eye.
The cellular physiology of the lens actively maintains its optical properties and inhibiting the Na/K/ATPase induces a myopic shift in vision similar to that observed clinically in patients who go on to develop cataract.
确定晶状体的细胞生理学是否积极维持晶状体的光学特性，以及抑制晶状体转运是否会影响整体视觉质量。
将一对牛晶状体中的一个置于人工房水（AAH）中培养，而另一个则在AAH-高钾或含0.1 mM哇巴因的AAH中培养4小时。然后在4.7特斯拉（T）高场小动物磁体中对晶状体对或整个摘除的眼球进行成像。从培养的晶状体中提取晶状体表面曲率、水含量的T1测量值以及水/蛋白质比率的T2测量值，而从整个眼睛中获取定义光路的几何参数。根据T2测量值计算的折射率梯度（GRIN）和提取的几何参数被输入到离体晶状体和整个牛眼的光学模型中。
用哇巴因抑制钠钾ATP酶来抑制循环通量，或用高钾使晶状体电位去极化，都会导致晶状体水含量、水/蛋白质比率（GRIN）和表面几何形状发生变化，表现为培养晶状体的屈光力增加和负球差减小。晶状体光学特性的变化导致近视偏移，损害了牛眼光学模型中的视觉质量。
晶状体的细胞生理学积极维持其光学特性，抑制钠/钾/ATP酶会导致视力出现近视偏移，类似于临床上白内障患者所观察到的情况。
