The Study On Retinal Injury And The Role Of Glutamate In Experimental Ocular Hypertension On Rabbits

Objective 1. To investigate the effects of pressure induced retinal ischemia on ERG in rabbit. 2. To monitor the release of amino acids of the whole retina during and after experimental glaucoma by increasing the intraocular pressure(IOP). Methods 1. Retinal ischemia was induced in rabbits by increasing intraocular pressure at 30mmHg, 60mmHg, 90mmHg, 120mmHg for 45min, and retinal function was monitored by electro-retinography. 2. experimental glaucoma was induced in one of the two eyes of rabbits by increasing TOP at 120mmHg for 45min; then the pressure was released and the needle inserted into the anterior chamber was removed, this state was maintained for another 45min. Every 15min during the experiment 5 rabbits were killed and experimental eyes were enucleared. Aliquots(10 jx l)of the retinal extracts(see below)were mixed with o-phthaldialdehyde reagent and analysed for amino acid content by the HPLC method of WangWei, using a 150x4.6mm, 5 JJL m C18 column.Results (1) In eyes subjected to 30mmHg ischemia, no difference was found between experimental eyes and before or control. In60mmHg pressure induced ischemia eyes, the amplitudes of the fa-wave and OPs wave reduced significantly. 4 hours after reperfusion, they were totally recovered. After an ischemic insult of 90mmHg or 120mmHg for 45min, there was no response of ERG. 4 hours later, the amplitudes of the b-wave and OPs wave were 66.912 ?20.157 and 16.423 ?.965 the former,38.852 ?23.438 and 8.610 ?12.090 the latter, respectively. (2) A large increase in the release of glutamate, but not of three other amino acids monitored, occurred during initial experimental ocular hypertension. It reached peak value of 111.73 ?17.46(10"5mMol/g)at 15min of hypertension. 5min after release of intraocular pressure, again, immediately large and specific increase in the concentration of glutamate was reached to 102.96 ?51.91(10" 5mMol/g). No significant variation was found at other time of the experiment and on other three amino acids. In eyes subjected to paracentesis of anterior chamber, no difference was found between experimental eyes and control.Conclusions (1) Higher intraocular pressure causes more severeretina ischemic damage, and less recovery ability. (2) Glutamaterelease can be triggered by increasing the IOP, and it releases notonly during the period of experimental ocular hypertension, but alsoafterwards.