外伤性前部PVR睫状体Na，K-ATP酶、碳酸酐酶活性测定及慢性低眼压视网膜结构和功能改变的实验研究
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摘要
目的
研究外伤性前部PVR后和房水产生密切相关的Na，K-ATP酶和碳酸酐酶活性变化，进一步深入探讨外伤性前部PVR导致慢性低眼压的机制：观察慢性低眼压后视网膜功能和结构变化，探讨可能的损伤机制。
方法
制作外伤性前部PVR导致慢性低眼压的兔眼模型，实验组角膜缘切口摘除晶状体核和部分皮质，11点和5点虹膜睫状体放射状剪开，让虹膜根部的血管自然出血，用截囊针反复划碎囊膜，并深入睫状体附近的玻璃体将出血、碎囊膜和剩余的少量晶状体皮质搅拌混入；对照组只做晶状体的囊外摘除。伤后分别于2周、4周、8周、16周测量眼压，进行暗适应视网膜电图检查后取眼球，部分睫状体和视网膜做普通病理切片，HE染色观察，部分睫状体做Na，K-ATP酶的活性测定和碳酸酐酶的组织化学观察，16周的视网膜部分做电镜观察。
结果
(1)眼压：伤后2周实验组的眼压比正常下降约15 mmHg，伤后4周到16周还有小幅下降，而对照组伤后2周的眼压比正常下降约10mmHg，伤后4周到16周变化不大，两组间比较有显著性差异；
(2)睫状体的病理学改变：伤后2周，实验组睫状突肿胀，睫状突
摘要
表面有纤维素样渗出，睫状上皮结构基本；厂常，而对照组睫状突肿胀，睫
状突表面有少量纤维素样渗出，睫状上皮结构基本正常：伤后4周、8周
和 16周，实验组睫状突肿胀逐渐消退，睫状突表面有比较多增殖的纤维条
索状物，睫状上皮许多区域结构紊乱，部分区域上皮可见萎缩，甚至上皮
，结构消失，而对照组睫状突表面有个别纤维样条索状物，睫状上皮结构基
本正常；外伤性前部PVR对睫状上皮的损害是不均一的，有的区域损害比
较重，而有的区域保持相对完好；
（3）Na，K－ATP酶和碳酸酸酶活性变化：伤后2周，实验组Na，K－ATP
酶的活性和正常相差不大，伤后 4周下降约 3 l．．－x－r－IPi／gprot／hour，伤后
8周和16周还有小幅下降，而对照组变化不很明显，两组问比较有显著性
的差异；碳酸酸酶组织化学显色，实验眼睫状体上皮部分区域为浓的棕黑
色，表明这部分上皮碳酸配酶活性接近正常水平，参照HE染色这部分为上
皮保持相对比较好的区域，而HE染色所见上皮破坏的区域，酶组织化学显
色比较弱，接近于阴性对照的睫状体上皮的颜色，为淡的黄褐色，表明这
部分上皮碳酸配酶活性较低；对照组睫状体上皮显色和正常的基本相同，
为浓的棕黑色，表明碳酸酸酶活性正常；
（4）视网膜电图的变化：伤后2周，实验组视网膜电图b波的振幅
高于正常，约为正常的2．5倍，伤后4周到16周逐渐下降，而对照组伤后
2周视网膜电图b波的振幅高于正常，约为正常的1．5倍，伤后4周到16
周逐渐下降，两组间比较有显著性差异；
J 乃）视网膜结构的变化：伤后 2周、4周、8周光学显微镜下，实
验组和对照组视网膜的显微结构均没有明显的变化；伤后16周，光学显微
镜下，实验组视网膜变薄，外核层、内核层以及节细胞细胞数减少，部分
细胞可见核浓缩，对照组没有明显的变化；伤后16周扫描电镜下见光感受
器外节排列紊乱，肿胀。
2
摘要
结论
门）外伤性前部PVR睫状体Na，K－ATP酶和碳酸配酶活性降低，是
导致房水分泌减少及慢性低眼压的一个重要原因；
（2）低眼压后视网膜电图b波高于正常，可能与低眼压造成视网膜
血液循环淤滞，代谢产物淤积有关；慢性低眼压对视网膜结构损害程度随
着时间的延长逐渐加重，主要为视网膜变薄，外核层、内核层以及节细胞
细胞数减少，光感受器外节肿胀、排列紊乱。
Study on Activity Changes of Na, K-ATPase and carbonic anhydrase of
Ciliary Body after Traumatic Anterior Proliferative Vitreoretinopathy and Retinal Structural and Functional Changes
after Chronic Hypotony
Objective: To study the changes of activity of two important enzymes related to the productivity of aqueous humor, namely Na, K-ATPase and carbonic anhydrase, and to probe more into the mechanism of traumatic anterior proliferative vitreoretinopathy inducing chronic hypotony. To observe the changes of retinal function and structure after traumatic chronic hypotony, and to discuss the possible mechanism of lesions.
Method: At first the rabbit model of chronic hypotony due to traumatic anterior proliferative vitreoretinopathy was made. In treated group, lens nucleus and some cortices were removed through a corneal limbus incision, and iris and ciliary body was cut radiatively at 11 and 5 o' clock to let the blood flow out naturly from the blood vessel in the root of iris. Capsule was broken into pieces by discission needle. Blood, capsule pieces and the remanent lens cortices were blended with vitreous near the ciliary bosy. In contrasted group, only the lens was removed by ECCE. At the 2nd week, 4th week, 8th
week, 16th week after trauma, IOP was measured and electroretinogram (ERG) was examined. Then eyeballs were removed and part of ciliary body and retina were taken for ordinary pathological section and HE staining, part of ciliary body was used for mensuration of Na, K-ATPase' s activity and histochemistry examination of carbonic anhydrase, part of retina at the 16th week after trauma was send for electron microscopy exam.
Result: (1)IOP: IOP of treated group decreased gradually after trauma,
while IOP of contrasted group decreased at the beginning, became
stable afterward. There is significant difference between two groups.
(2) Pathological changes of ciliary body: At the 2nd week after
trauma, in treated group, the ciliary process is swelling and there
is fibrinoid exudation on the surface of ciliary process, while the
structure of the pigmental and nonpigmental epithelia is normal. In
contrasted group, the ciliary process is also swelling and there is
less fibrinoid exudation on the surface of ciliary process. The
structure of the pigmental and nonpigmental epithelia is normal. At
the 4th week after trauma, in treated group, there is still a little
ciliary body swelling, and proliferated fibriform matter can be seen
on the surface of ciliary process, but structure of the pigmental
and nonpigmental epithelia is nearly normal. In contrasted group,
there is no ciliary body swelling, and there is little proliferated
fibriform matter on the surface of ciliary process. At the 8th and
16th week after trauma, in treated group, there is nearly no ciliary
body swelling, and much proliferated fibriform matter can be seen on the surface of ciliary process, and parts of the pigmental and nonpigmenta epithelia have disordered structure, even some parts are atrophy or disappeared. In contrasted group, there are little proliferated fibriform matter on the surface of ciliary process and ciliary epithelia are normal. The lesions of ciliary epithelia by traumatic anterior proliferative vitreoretinopathy are not equal in every part. Some parts got heavy lesions and the structure of epithelia is disordered or atrophy, even disaooeared, while some parts are nearly normal. (3) Changes of activity of Na, K-ATPase and carbonic anhydrase: Activity of Na, K-ATPase decreased gradually in treated group but there is no remarkable decrease in contrasted group. There is significant difference between two groups. In treated group the colour of some ciliary epithelia were thick brownish black after histochemistry examination of carbonic anhydrase performed, indicating the activity of carbonic anhydrase is nearly normal. These parts are nearly normal epithelia when contrasted to HE stained section. But the destroyed epithelia were mild yellowish brown, indicating the activity o
研究外伤性前部PVR后和房水产生密切相关的Na，K-ATP酶和碳酸酐酶活性变化，进一步深入探讨外伤性前部PVR导致慢性低眼压的机制：观察慢性低眼压后视网膜功能和结构变化，探讨可能的损伤机制。
方法
制作外伤性前部PVR导致慢性低眼压的兔眼模型，实验组角膜缘切口摘除晶状体核和部分皮质，11点和5点虹膜睫状体放射状剪开，让虹膜根部的血管自然出血，用截囊针反复划碎囊膜，并深入睫状体附近的玻璃体将出血、碎囊膜和剩余的少量晶状体皮质搅拌混入；对照组只做晶状体的囊外摘除。伤后分别于2周、4周、8周、16周测量眼压，进行暗适应视网膜电图检查后取眼球，部分睫状体和视网膜做普通病理切片，HE染色观察，部分睫状体做Na，K-ATP酶的活性测定和碳酸酐酶的组织化学观察，16周的视网膜部分做电镜观察。
结果
(1)眼压：伤后2周实验组的眼压比正常下降约15 mmHg，伤后4周到16周还有小幅下降，而对照组伤后2周的眼压比正常下降约10mmHg，伤后4周到16周变化不大，两组间比较有显著性差异；
(2)睫状体的病理学改变：伤后2周，实验组睫状突肿胀，睫状突
摘要
表面有纤维素样渗出，睫状上皮结构基本；厂常，而对照组睫状突肿胀，睫
状突表面有少量纤维素样渗出，睫状上皮结构基本正常：伤后4周、8周
和 16周，实验组睫状突肿胀逐渐消退，睫状突表面有比较多增殖的纤维条
索状物，睫状上皮许多区域结构紊乱，部分区域上皮可见萎缩，甚至上皮
，结构消失，而对照组睫状突表面有个别纤维样条索状物，睫状上皮结构基
本正常；外伤性前部PVR对睫状上皮的损害是不均一的，有的区域损害比
较重，而有的区域保持相对完好；
（3）Na，K－ATP酶和碳酸酸酶活性变化：伤后2周，实验组Na，K－ATP
酶的活性和正常相差不大，伤后 4周下降约 3 l．．－x－r－IPi／gprot／hour，伤后
8周和16周还有小幅下降，而对照组变化不很明显，两组问比较有显著性
的差异；碳酸酸酶组织化学显色，实验眼睫状体上皮部分区域为浓的棕黑
色，表明这部分上皮碳酸配酶活性接近正常水平，参照HE染色这部分为上
皮保持相对比较好的区域，而HE染色所见上皮破坏的区域，酶组织化学显
色比较弱，接近于阴性对照的睫状体上皮的颜色，为淡的黄褐色，表明这
部分上皮碳酸配酶活性较低；对照组睫状体上皮显色和正常的基本相同，
为浓的棕黑色，表明碳酸酸酶活性正常；
（4）视网膜电图的变化：伤后2周，实验组视网膜电图b波的振幅
高于正常，约为正常的2．5倍，伤后4周到16周逐渐下降，而对照组伤后
2周视网膜电图b波的振幅高于正常，约为正常的1．5倍，伤后4周到16
周逐渐下降，两组间比较有显著性差异；
J 乃）视网膜结构的变化：伤后 2周、4周、8周光学显微镜下，实
验组和对照组视网膜的显微结构均没有明显的变化；伤后16周，光学显微
镜下，实验组视网膜变薄，外核层、内核层以及节细胞细胞数减少，部分
细胞可见核浓缩，对照组没有明显的变化；伤后16周扫描电镜下见光感受
器外节排列紊乱，肿胀。
2
摘要
结论
门）外伤性前部PVR睫状体Na，K－ATP酶和碳酸配酶活性降低，是
导致房水分泌减少及慢性低眼压的一个重要原因；
（2）低眼压后视网膜电图b波高于正常，可能与低眼压造成视网膜
血液循环淤滞，代谢产物淤积有关；慢性低眼压对视网膜结构损害程度随
着时间的延长逐渐加重，主要为视网膜变薄，外核层、内核层以及节细胞
细胞数减少，光感受器外节肿胀、排列紊乱。
Study on Activity Changes of Na, K-ATPase and carbonic anhydrase of
Ciliary Body after Traumatic Anterior Proliferative Vitreoretinopathy and Retinal Structural and Functional Changes
after Chronic Hypotony
Objective: To study the changes of activity of two important enzymes related to the productivity of aqueous humor, namely Na, K-ATPase and carbonic anhydrase, and to probe more into the mechanism of traumatic anterior proliferative vitreoretinopathy inducing chronic hypotony. To observe the changes of retinal function and structure after traumatic chronic hypotony, and to discuss the possible mechanism of lesions.
Method: At first the rabbit model of chronic hypotony due to traumatic anterior proliferative vitreoretinopathy was made. In treated group, lens nucleus and some cortices were removed through a corneal limbus incision, and iris and ciliary body was cut radiatively at 11 and 5 o' clock to let the blood flow out naturly from the blood vessel in the root of iris. Capsule was broken into pieces by discission needle. Blood, capsule pieces and the remanent lens cortices were blended with vitreous near the ciliary bosy. In contrasted group, only the lens was removed by ECCE. At the 2nd week, 4th week, 8th
week, 16th week after trauma, IOP was measured and electroretinogram (ERG) was examined. Then eyeballs were removed and part of ciliary body and retina were taken for ordinary pathological section and HE staining, part of ciliary body was used for mensuration of Na, K-ATPase' s activity and histochemistry examination of carbonic anhydrase, part of retina at the 16th week after trauma was send for electron microscopy exam.
Result: (1)IOP: IOP of treated group decreased gradually after trauma,
while IOP of contrasted group decreased at the beginning, became
stable afterward. There is significant difference between two groups.
(2) Pathological changes of ciliary body: At the 2nd week after
trauma, in treated group, the ciliary process is swelling and there
is fibrinoid exudation on the surface of ciliary process, while the
structure of the pigmental and nonpigmental epithelia is normal. In
contrasted group, the ciliary process is also swelling and there is
less fibrinoid exudation on the surface of ciliary process. The
structure of the pigmental and nonpigmental epithelia is normal. At
the 4th week after trauma, in treated group, there is still a little
ciliary body swelling, and proliferated fibriform matter can be seen
on the surface of ciliary process, but structure of the pigmental
and nonpigmental epithelia is nearly normal. In contrasted group,
there is no ciliary body swelling, and there is little proliferated
fibriform matter on the surface of ciliary process. At the 8th and
16th week after trauma, in treated group, there is nearly no ciliary
body swelling, and much proliferated fibriform matter can be seen on the surface of ciliary process, and parts of the pigmental and nonpigmenta epithelia have disordered structure, even some parts are atrophy or disappeared. In contrasted group, there are little proliferated fibriform matter on the surface of ciliary process and ciliary epithelia are normal. The lesions of ciliary epithelia by traumatic anterior proliferative vitreoretinopathy are not equal in every part. Some parts got heavy lesions and the structure of epithelia is disordered or atrophy, even disaooeared, while some parts are nearly normal. (3) Changes of activity of Na, K-ATPase and carbonic anhydrase: Activity of Na, K-ATPase decreased gradually in treated group but there is no remarkable decrease in contrasted group. There is significant difference between two groups. In treated group the colour of some ciliary epithelia were thick brownish black after histochemistry examination of carbonic anhydrase performed, indicating the activity of carbonic anhydrase is nearly normal. These parts are nearly normal epithelia when contrasted to HE stained section. But the destroyed epithelia were mild yellowish brown, indicating the activity o
引文
1. Kim HC, Hayashi A, Shalash A, de Juan E Jr. A model of chronic hypotony in the rabbit. Graefes Arch Clin Exp Ophthalmol, 1998;236:69-74
2. Milton Best, Tonometric calibration for the rabbit eye, Arch ophthal, 1970;84,8:200-205
3． 王强，魏厚仁，樊郑军，家兔眼压测量的标定问题，眼科研究，1994；12：224-226
4． 张卯年，外伤性低眼压，国外医学眼科学分册，1986；10：143-146
5. Paster JC. Proliferative Vitrectoretinopathy: An Overview. Survey of Ophthalmology. 1998;43:3
6. O'Connell SR, Majji AB, Humayun MS, de Juan E Jr, The surgical management of hypotony. Ophthalmology 2000;107:318-23
7. Marak CE, et al. Immunopathogenicity of lens crystallins in the production of experimental lensinduceced grunulomatous endophthalmitis. Ophthalmol Res, 1978, 10:30
8． 赵伟，晶体源性眼内炎发病机理的实验研究。眼科研究，1990，8：38
9． 张效房，杨进献，眼外伤学，郑州：河南医科大学出版社，1997年，406页
2. Milton Best, Tonometric calibration for the rabbit eye, Arch ophthal, 1970;84,8:200-205
3． 王强，魏厚仁，樊郑军，家兔眼压测量的标定问题，眼科研究，1994；12：224-226
4． 张卯年，外伤性低眼压，国外医学眼科学分册，1986；10：143-146
5. Paster JC. Proliferative Vitrectoretinopathy: An Overview. Survey of Ophthalmology. 1998;43:3
6. O'Connell SR, Majji AB, Humayun MS, de Juan E Jr, The surgical management of hypotony. Ophthalmology 2000;107:318-23
7. Marak CE, et al. Immunopathogenicity of lens crystallins in the production of experimental lensinduceced grunulomatous endophthalmitis. Ophthalmol Res, 1978, 10:30
8． 赵伟，晶体源性眼内炎发病机理的实验研究。眼科研究，1990，8：38
9． 张效房，杨进献，眼外伤学，郑州：河南医科大学出版社，1997年，406页