Influence of arterial hypertension and diet-induced atherosclerosis on macular drusen
Influence of arterial hypertension and diet-induced atherosclerosis on macular drusen
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DOI：
10.1007/s00417-002-0615-3
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发表时间：
2003-02-01
影响因子：
2.7
通讯作者：
Martus, P
中科院分区：
文献类型：
--
作者：
Jonas, JB;Hayreh, SS;Martus, P
目的：评价实验性慢性动脉高压和动脉粥样硬化是否影响黄斑玻璃疣的发生。方法：对51只老年恒河猴的93只眼进行前瞻性实验研究。总研究组分为实验性动脉高血压组。（n=22），饮食诱导的动脉粥样硬化（n=10），或动脉高血压和动脉粥样硬化（n=29）和对照组无动脉高血压或动脉粥样硬化（n=32）。使用在研究开始和结束时拍摄的彩色广角眼底照片，通过计数黄斑区玻璃疣的数量和估计玻璃疣的平均大小对年龄相关性黄斑变性进行分级。结果如下：在患有动脉高血压的猴中，黄斑玻璃疣的计数和面积以及随访期间黄斑玻璃疣的数量和大小的变化与动脉粥样硬化的持续时间显著无关（P0.20）。同样，动脉粥样硬化猴和对照组猴在随访期间黄斑玻璃疣参数的变化也无显著性差异（P>0.30）。结论恒河猴老年性黄斑变性黄斑玻璃疣的发生可能与实验性动脉高压有关。它似乎不受饮食诱导的动脉粥样硬化的影响。
Purpose: To evaluate whether development of macular drusen is influenced by experimentally induced chronic arterial hypertension and atherosclerosis. Methods: The prospective experimental study included 93 eyes of 51 elderly rhesus monkeys. The total study group was divided into groups with experimental arterial hypertension. (n=22), diet-induced atherosclerosis (n=10), or both arterial hypertension and atherosclerosis (n=29) and a control group without arterial hypertension or atherosclerosis (n=32). Using color wide-angle fundus photographs taken at the beginning and the end of the study, age-related macular degeneration was graded by counting the number and estimating the mean size of drusen in the macular region. Results: In the monkeys with arterial hypertension, the count and area of the macular drusen and the change in number and size of macular drusen during the follow-up period were significantly (P0.20) independent of the duration of atherosclerosis. Similarly, the atherosclerotic monkeys and the monkeys of the control group did not vary significantly (P>0.30) in the change of the macular drusen parameters during the follow-up period. Conclusions Development of macular drusen as part of age-related macular degeneration in rhesus monkeys may be associated with experimentally induced arterial hypertension. It does not seem to be influenced by diet-induced atherosclerosis.