Objective To monitor the release of amino acids of the whole retina during and after experimental glaucoma by increasing the intraocular pressure （IOP）． Methods Experimental glaucoma was induced in one of the two eyes of rabbits by increasing IOP at 120 mm Hg for 45 min under infusion of saline in anterior chamber；then the pressure was released and the needle inserted into the anterior chamber was removed，this state was maintained for another 45 min．Every 15 min during the experiment 5 rabbits were killed and experimental eyes were enucleated．Aliquots（20 μl）of the retinal extracts（see below）were mixed with ophthaldialdehyde reagent and analysed for amino acid content by the HPLC method of Wangwei，using a 150 mm×4.6 mm,5 μm C18 column． Results A large increase in the release of glutamate，but not of the other three amino acids monitored，occurred during initial experimental ocular hypertension．It reached peak value of（111.73±17.46）10-5 mmol/g at 15 min of hypertension．15 min after release of intraocular pressure，again，immediately large and specific increase in the concentration of glutamate was reached to（102.96±51.91）10-5 mmol/g．In eyes subjected to paracentesis of anterior chamber，no difference was found between experimental eyes and controls. Conclusion These results suggest that glutamate is triggered by increasing the IOP，and it releases not only during the period of experimental ocular hypertension，but also afterwards. (Chin J Ocul Fundus Dis, 2002, 18: 146-148)
Objective To investigate the risk factors of the intraocular pressure (IOP) elevation after pars plana vitrectomy (PPV). Methods Eighty-eight patients (88 eyes) of postoperative ocular hypertension in a series of 339 patients who had undergone PPV with normal ocular pressure before operation were retrospectively studied. The ocular pressures in both preoperative and postoperative periods were detected by NCT examination, and the ocular hypertension was decided on the level of ≥25 mm Hg. The relationships of occurence of the time of onset and duration of persistence of postoperative ocular hypertension with the different kinds of primary diseases, the techniques of operation, and the condition whether or not the affected eyes had formerly accepted surgical intervention, were analyzed. Results The IOP elevation occures mostly within 1 to 2 weeks postoperatively (77 eyes, 87.5%). In 65 cases (65 eyes) IOP returned to normal in 1 week, and in another 14 cases (14 eyes) in 1 month after treatments. Six patients’ (6 eyes ) IOP was under 25 to 30 mm Hg with the medicine. With sustained elevation of IOP over 4 to 6 months, 3 cases (3 eyes ) lost or almost lost their vision finally. The probability of postoperative IOP elevation in the patients suffered from the retinal detachment with proliferative vitreoretinopathy (PVR) ≥grade C-2 was the highest in all the patients in our study (38.2%, P＜0.05). The patients who had intraocular surgery before were more likely to have IOP elevation than the ones without intraocular surgery (P＜0.05). Placement of a scleral buckle, use of expansile gases or silicone oil injection and scatter endophotocoagulation intraoperatively were related to the postvitrectomy IOP elevation (γ=0.829, P＜0.001). Conclusions The previous intraocular surgeries, certain primary eye diseases and combined ocular procedures are the risk factors of IOP elevation after PPV. (Chin J Ocul Fundus Dis, 2002, 18: 106-108)
Objective To analyse the changes of nitric oxide and nitric oxide synthase in rat retina under acute high ocular pressure and study the effect of nitric oxide in rat retinal damage under hypertension. Methods Sixty Wistar rats were divided randomly into five groups:Ocular hypertension 30 min,60 min,90 min and 12 h,24 h after reperfusion．Elevation of the ocular pressure in the anterior chamber of the rat eye ca used retina ischemic damage．The changes of retinal nitric oxide content were ob served indirectly by measuring NO2－/NO3－ content in retina.The distribution and changes of neuronal constitutive nitric oxide synthase (ncNOS)were studied by immunocytochemical localization of ncNOS. Results ncNOS positive neurons were distributed in the inner nuclear layer (INL),ganglion cell layer (GCL) and the inner plexiform layer of the normal and ischemic rat retina.During acute high IOP 30 min,60 min and 90 min,NO content decreased gradually and ncNOS immune activity weakens.During reperfusion,NO content increased remarkably (Plt;0.05) as compared with the groups of hypertension 90 min and decreased remarkably as compared with the normal rat retina.But ncNOS positive neurons continue to decrease compared with the groups of hypertension 90 min. Conclusion NO participates the rat retinal injury by acute elevated intraocular pressure, and nitric oxide synthetized by ncNOS may play an important role in protecting the retina from ischemic and post-ischemic injury.