Abstract
PURPOSE: To explore the changes in vitreous body after vitreous hemorrhage and assess its prognosis from the perspective of vitreoretinal interface. METHODS: The experiment was performed on 32 New Zealand rabbits (64 eyes), weighing 2500-3000 g for 4 months and unlimited gender, which was injected with 0.2 mL of autologous blood into the center of vitreous cavity-the study group (right eyes), and the control one was treated in the same manner with equal volumes of saline. The rabbits were randomly and equally divided into the following four batches according to the days of observation: Days 3, 7, 14, and 30 after injection. IOP and severity grading were evaluated before rabbits' execution and eyeballs were enucleated. The anterior segment was separated to flow out the vitreous body naturally to detect the liquefaction degree and viscosity. Then, chemical composition of electrolytes, PCT and bFGF were determined by colorimetry and enzyme-linked immunosorbent assay (ELISA). Finally, the incidence of posterior vitreous detachment (PVD) was observed after vitreous sampled. The studies were double-blind. RESULTS: After injection, the extent of vitreous opacity and coagulum size decreased over time. Both the degree of liquefaction and the length of tow differed significantly between two groups at different time points (all p < 0.001). The liquefaction degree in the study group rose obviously from the Day 14, which the viscosity declined significantly on the initial time. Biochemical markers fluctuated temporarily, except for basic fibroblast growth factor (bFGF), which continued to rise and was correlated with the liquefaction degree (r = 0.658, p < 0.001). Besides, the incidence of PVD increased from the 14th day (p < 0.05), and it was highly positively correlated with the number of macrophages (r = 0.934; p < 0.001). CONCLUSION: After vitreous hemorrhage, the changes of the vitreous body are relatively minor earlier (2-4 weeks), but irreversible later. Specifically, the degree of liquefaction increases with a decrease in viscosity, and the chemotaxis of macrophages and bFGF induce incomplete PVD.