【Disease Animal Model】-Oxygen-induced retinal neovascularization model

  [Modeling mechanism] Oxygen induces retinal neovascularization. Pathological angiogenesis is accompanied by abnormal vascular buds that crawl from the retina to the vitreous. This new blood vessel sprouting can cause many complications, such as plasma leakage, bleeding, and in some cases retinal detachment or blindness. In the first stage of hyperoxia exposure (7-12 days after birth), retinal blood vessels contract to regulate the oxygen partial pressure of the retina, while the immature capillaries in the central part of the retina degenerate and cause blood vessels. section. Due to the high oxygen exposure and the physiologically vertical vascular sprout, it grows from the superficial capillary network to the deep layer. This significantly delayed the formation of the deep capillary network of the retina. In the second stage, after returning to normal air conditions at the age of 12 days, the vascular occlusion area began to become hypoxic, and there was no blood vessel or pathological angiogenesis in the retinal vascular occlusion area of the mouse. [Modeling method] The oxygen chamber for supplying oxygen to mice and their mothers is used for animals with an oxygen concentration of 75%±2% for a period of 5 days and lasts for 1 week. The oxygen flow rate in the oxygen chamber is controlled at 0.5-0.6L/min, and the exhaust flow rate can be adjusted by itself to ensure oxygen circulation, and the concentration is stable at about 75%. After the oxygen concentration in the oxygen reaches a certain value, the chamber will remain stable and use this value every 4 hours. The oxygen meter monitors the oxygen concentration in the oxygen chamber to check the balance between the inflow and outflow of gas. The pressure in the oxygen chamber should be maintained at or near atmospheric pressure. Then feed under normal air conditions for 5 days.

  [Model Features] Under normal air conditions, after 5 days of oxygen induction and 5 days of rearing, C57BL/6J mice showed obvious vascular contracture or dilation, flexion and sparse distribution. The non-perfusion area is mainly concentrated in the central part of the retina, with new blood vessels or scattered bleeding in the surrounding parts. At the age of 17 days, the oxygen-induced mice had a large number of vascular endothelial cells, which broke through the inner restrictive membrane of the retina, and some even formed a network of blood vessels that reached the vitreous. However, in normal mouse retinal tissue sections, almost no vascular endothelial cell nuclei that penetrated the inner restrictive membrane were observed at the age of 17 days. Oxygen-induced anti-VEGF immunohistochemical staining of mouse retina was enhanced. [Model Evaluation and Application] Oxygen-induced retinal neovascularization simulates the exposure of premature infants to normal partial pressure of oxygen and may cause retinal diseases in premature infants, which provides experimental basis for research on diagnosis and treatment methods. During the modeling process, large air intake and exhaust ports can be opened every day for complete ventilation to ensure the viability of the mouse after leaving the cabin. Will produce toxic and harmful gases produced by the metabolism of laboratory animals. Re-adjust the oxygen flow rate to keep it under the experimental concentration conditions so as to completely exhaust oxygen and discharge water vapor. Frequent ventilation is required, especially in summer. If the female mouse died during the experiment, the spare female mouse was opened for breastfeeding. The lactobacilli that replaced female mice can be used to completely cover and smear offspring to prevent breastfeeding or non-lactation of offspring.