Gundorova R A, Ivanov A N, Tsapenko I V, Zueva M V, CHesnokova N B, Shvetsova N E, Beznos O V, Stoliarova E P, Andersen E B
Vestn Oftalmol. 2007 Sep-Oct;123(5):28-32.
The pattern of functional impairments and the antioxidative and antiproteolytic status of tear were studied, by experimentally simulating retinal ischemia in rabbits and during treatment with Selecarten. Simulated retinal ischemia resulted in the development of persistent (up to 3 weeks) retinal electrogenetic disorder. Selecarten instillations produced a moderate neuroprotective effect, by positively affecting retinal function early after ischemia stimulation and accelerated the recovery of retinal electrogenesis late after laser coagulation of retinal vessels. The altered metabolic processes were characterized by an increase in the tear antiproteolytic potential. The antioxidative activity and the activity of a2-macroglobulin proteolysis inhibitor increased in the tears of Selecarten-treated rabbits.
通过在兔子身上实验性模拟视网膜缺血以及在使用Selecarten治疗期间，研究了泪液的功能损伤模式以及抗氧化和抗蛋白水解状态。模拟视网膜缺血导致持续性（长达3周）视网膜电发生紊乱。Selecarten滴眼产生了适度的神经保护作用，通过在缺血刺激后早期对视网膜功能产生积极影响，并在视网膜血管激光凝固后晚期加速视网膜电发生的恢复。代谢过程的改变表现为泪液抗蛋白水解潜力增加。在接受Selecarten治疗的兔子的泪液中，抗氧化活性和α2-巨球蛋白蛋白水解抑制剂的活性增加。
