Ozerdem U, Mach-Hofacre B, Cheng L, Chaidhawangul S, Keefe K, McDermott C D, Bergeron-Lynn G, Appelt K, Freeman W R
Shiley Eye Center, University of California, San Diego, California 92093-0946, United States of America.
Curr Eye Res. 2000 Jun;20(6):447-53.
To determine the efficacy of prinomastat (AG3340), a synthetic inhibitor of matrix metalloproteinase, in the treatment of experimental proliferative vitreoretinopathy (PVR) induced by intravitreal dispase injection.
One eye each of 53 New Zealand white rabbits was injected in the vitreous cavity with 0.07 unit of dispase to induce PVR. One week after PVR induction, 53 rabbits were randomized (27:26) to receive 0.5 mg prinomastat or the vehicle of the drug (acidified water) intravitreally every two weeks. The scores of PVR severity (scale of 1-5) were graded to compare the prinomastat-treated animals with the control group.
The average PVR scores in the treatment and control groups were 2.62 and 3.57 respectively (p = 0.038; Wilcoxon rank sum). Clinically significant PVR with retinal detachment (PVR > or = grade 3) developed in 76% of rabbits in the control group versus 51% of rabbits treated with prinomastat.
Intravitreally administered prinomastat decreased development of PVR in an experimental model which made use of dispase to induce PVR.
确定基质金属蛋白酶合成抑制剂普林司他（AG3340）治疗玻璃体内注射分散酶诱导的实验性增殖性玻璃体视网膜病变（PVR）的疗效。
给53只新西兰白兔的每只一眼玻璃体内注射0.07单位分散酶以诱导PVR。诱导PVR一周后，将53只兔子随机分为两组（27只：26只），分别每两周玻璃体内注射0.5毫克普林司他或药物载体（酸化水）。对PVR严重程度进行评分（1 - 5级），以比较普林司他治疗组动物与对照组。
治疗组和对照组的平均PVR评分分别为2.62和3.57（p = 0.038；Wilcoxon秩和检验）。对照组76%的兔子发生了伴有视网膜脱离的具有临床意义的PVR（PVR≥3级），而普林司他治疗组为51%。
在利用分散酶诱导PVR的实验模型中，玻璃体内注射普林司他可减少PVR的发生。
