摘要
目的 研究外伤性前部增生性玻璃体视网膜病变 (aPVR)睫状体Na+ K+ ATP酶和碳酸酐酶活性变化 ,进一步深入探讨外伤性aPVR导致慢性低眼压的机制。方法 制作外伤性aPVR导致慢性低眼压兔眼模型 ,分别于伤后 2、4、8、16周测量眼压后取眼球 ,部分睫状体做普通病理切片 ,HE染色观察 ,部分睫状体做Na+ K+ ATP酶活性测定和碳酸酐酶组织化学观察。结果 伤后实验组Na+ K+ ATP酶活性下降 ,而对照组变化不很明显 ,两组间比较有显著性差异 ;实验眼睫状体上皮碳酸酐酶部分区域活性接近正常水平 ,而上皮破坏区域 ,酶活性较低。结论 外伤性aPVR睫状体Na+ K+ ATP酶和碳酸酐酶活性降低是导致房水分泌减少及慢性低眼压的一个重要原因。
Objective To study the changes in the activity of two important enzymes related to the productivity of aqueous humor, namely Na +-K +ATPase and carbonic anhydrase, and to probe further into the mechanism of induction of chronic ocular hypotony by traumatic anterior proliferative vitreoretinopathy. Methods A rabbit model of chronic hypotony induced by traumatic anterior proliferative vitreoretinopathy was reproduced. At the 2nd , 4th, 8th and 16th week after trauma, IOP was measured. Then eyeballs were removed, and a part of ciliary body was harvested for orthodox pathological section and HE staining, and another part of ciliary body was used for determination of Na +-K +ATPase's activity and histochemical assessment of carbonic anhydrase. Result Activity of Na, K-ATPase decreased gradually in the experimental group, but there is no remarkable change in the control group, and the difference was significant. In the experimental group, the activity of carbonic anhydrase was nearly normal, but the activity of carbonic anhydrase in the area of injured epithelium was low, and it was similar to the control. Conclusion Activity of ciliary Na +-K +-ATPase and carbonic anhydrase decrease in activity after traumatic anterior proliferative vitreoretinopathy, which is an important causative factor of chronic hypotony.
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2005年第2期114-116,共3页
Medical Journal of Chinese People's Liberation Army
基金
全军"十五"医学科研面上项目资助课题 (编号 0 1MA1 1 3)
