Manganese-enhanced MRI studies of alterations of intraretinal ion demand in models of ocular injury
Manganese-enhanced MRI studies of alterations of intraretinal ion demand in models of ocular injury
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DOI：
10.1167/iovs.06-1278
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发表时间：
2007-08-01
影响因子：
4.4
通讯作者：
Vingrys, Algis J.
中科院分区：
文献类型：
--
作者：
Berkowitz, Bruce A.;Roberts, Robin;Vingrys, Algis J.
目的.为了提供概念验证，即通过锰增强MRI（MEMRI）检测全身性MnCl 2注射后视网膜内锰摄取的程度，评估眼损伤模型中视网膜内离子需求的改变。在Sprague-Dawley大鼠中，视网膜离子需求和厚度从MEMRI数据收集前，4小时后，或1，3，7天后腹腔注射氯化锰。在注射Gd-DTPA后，使用MRI确定脉络膜贡献或血-视网膜屏障通透性表面积乘积（BRB PS '）。在玻璃体内注射磷酸盐缓冲盐水（PBS，载体）或PBS +哇巴因后24小时，或在腹膜内注射碘酸钠后，评价眼损伤。通过比较全身性MnCl 2给药前后获得的全视野白光视网膜电图（ERG）数据，评估锰的视网膜毒性。大鼠脉络膜厚度测量制备的横截面从多聚甲醛灌注成年大鼠。对比Gd-DTPA检查前后的图像显示脉络膜对视网膜内分析的贡献最小。视网膜内信号强度在MnCl 2注射后7天恢复至基线。注射哇巴因后，受体和受体后锰摄取均低于正常（P < 0.05）。碘酸钠暴露后，视网膜内锰摄取量明显高于正常（P < 0.05），且不随BRB PS '的增加而增加。在两个观察时间点，ERG数据均未显示MnCl 2对感光细胞a波和受体后b波相对于基线的任何影响。MEMRI测量全身给药和无毒剂量的锰的摄取似乎是一个强大的方法来测量眼损伤模型中视网膜内离子需求的改变。
PURPOSE. To provide proof-of-concept that the extent of intraretinal manganese uptake after systemic MnCl2 injection, detected with manganese-enhanced MRI (MEMRI), assesses alterations in intraretinal ion demand in models of ocular insult.METHODS. In Sprague-Dawley rats, retinal ion demand and thickness were measured from MEMRI data collected before, 4 hours after, or 1, 3, and 7 days after intraperitoneal injection of MnCl2. Choroidal contribution or blood-retinal barrier permeability surface area product (BRB PS') was determined using MRI after Gd-DTPA injection. Ocular injury was evaluated 24 hours after intravitreal injection of phosphate-buffered saline (PBS, vehicle) or PBS + ouabain, or after intraperitoneal injection of sodium iodate. Manganese retinal toxicity was assessed by comparing full-field, white-flash electroretinographic (ERG) data obtained before and after systemic MnCl2 administration. Rat choroidal thickness was measured from cross-sections prepared from paraformaldehyde-perfused adult rats.RESULTS. Comparing pre- and post-Gd-DTPA images demonstrated minimal choroidal contribution to intraretinal analysis. Intraretinal signal intensity returned to baseline by 7 days after MnCl2 injection. After ouabain injection, receptor and postreceptor uptake of manganese were subnormal (P < 0.05). After sodium iodate exposure, intraretinal manganese uptake was supernormal (P < 0.05) and did not increase with increasing BRB PS'. ERG data did not show any effect of MnCl2 on photoreceptor a-wave and postreceptor b-wave relative to baseline at either observation time.CONCLUSIONS. MEMRI measurements of uptake of systemically administered and nontoxic doses of manganese appear to be a powerful approach for measuring alteration in intraretinal ion demand in models of ocular injury.