Study Of Protection And Mechanism Of Taurine On Acute Hypoxia Induced Rat Retina Damage

In high altitude area over 3 000 meters, body physiological function changes to adapt to hypobaric hypoxia. Acutely advancing to plateau, high altitude response and altitude illness(AI) occur in 80%～90% people. High altitude hypoxia has effects on visual function, for example, dark adaptation time prolonged, vision decreased, color vision decreased, severely retinal hemorrhage. Retinal damage at high altitude is called high-altitude retinopathy(HAR). The symptoms of HAR are anapetia and haemorrhage, some of which induced visual functional disturbance or loss of sight, some of sufferers can not recover back to plain.Oxygen transport of outer layer of retina relies on blood capillary, and oxygen transport of inner layer is supported by retinal Müller cell. Müller cells are the principal glial cells in retina, and their nuclei locate in inner nuclear layer(INL), and the synapses extend from external limiting membrane to internal limiting membrane, in which blood-retina barriers are formed. Besides supporting and nutritional function, Müller cells act as retina homeostasis regulator. Hypoxia induces Müller cells functional degression and homeostasis disorder overall. Hypoxia induces exitotoxicity in neurons of retina inner layer. The continuous excitatory neurotransmitter glutamate affects retinal neurons, especially the retinal ganglion cells, ultimately leads to retinal ganglion cell apoptosis or death. Then visual signal transmission is blocked. Müller cells are the regulon of retinal glutamate. glutamate transporter 1(GLAST) in Müller cells transport redundant glutamate in synapse grudge,then convert them to glutamine by glutamine synthetase(GS), which is called glutamate cycle in retina. Glutamate transmission depends on K+ voltage. As glutamate are transported to cells, K+ go out. Hypoxia induces high concentration of K+ outside Müller cells, which inhibit glutamate uptake. Clearance of excessive K+ depends on inwardly rectifying K+ channel Kir4.1. The roles of glutamate-induced excitotoxicity were studied in retina. Further investigation of glutamate uptake and metablism in Müller cell at hypoxia is needed. Adaptation to hypoxia is an important pathway to hypoxia. Enhanced hypoxia...