Objective To observe the effect of lowering intraocular pressure(IOP) treatment on ocular hemodynamics in patients with nonarteritic anterior ischemic optic neuropathy (NAION). Methods A total of 68 patients with NAION (68 eyes) were enrolled in this study. The patients were randomly divided into treatment group (38 eyes of 38 patients) and control group (30 eyes of 30 patients). All the patients were received methylprednisolone pulse therapy (200 mg, three days), vasodilator therapy with intravenous infusion of Xueshuantong solution (300 mg), optic nerve nutritional therapy with mouse nerve growth factor (30 mu;g) and acupoint injection in temporal with compound anisodine (2 ml). The total course was 10 days. The patients of treatment group received IOP lowering treatment to reduce the IOP to ge;8 mm Hg (1 mm Hg=0.133 kPa) or in a 30% reduction. The patients of control group received no IOP lowering treatment. The peak systolic velocity (PSV), pulsatility index (PI) and resistance index (RI) of ophthalmic artery (OA), central retinal artery (CRA) and short posterior ciliary arteries (PCA) before and after treatment were comparatively analyzed by color doppler flow imaging. Results The differences of PSV (t=1.023, 1.145, 0.569), PI (t=0.679, 0.956, 1.634) and RI (t=0.816, 1.657, 0.998) of OA, CRA and PCA before treatment in treatment group and control group were not statistically significant (P＞0.05). Compared with before treatment, PSV (t=3.150, 7.650, 3.520) and PI (t=2.420, 5.430, 7.650) of OA, CRA and PCA increased obviously (P＜0.05), RI of OA, CRA and PCA decreased obviously (t=5.320, 9.640, 18.360;P＜0.05) after treatment in treatment group. In control group, the differences of PSV (t=2.090, -2.550, -2.100) and PI (t=-2.310, -2.230, -4.490) of OA, CRA and PCA between before and after treatment were not statistically significant (P＞0.05); but the differences of RI of OA, CRA and PCA between before and after treatment was statistically significant (t=2.970, 2.160, 2.690;P＜0.05). Compared with control group, PSV (t=2.632, 2.135, 5.364) and PI (t=3.251, 2.432, 4.243) of OA, CRA and PCA increased obviously (P＜0.05), RI of OA, CRA and PCA decreased obviously (t=3.664, 2.938, 4.324;P＜0.05) after treatment in treatment group. Conclusion Lowering intraocular pressure treatment can improve the ocular hemodynamics in NAION patients.
Objective To investigate the effect of proanthocyanidins (PC) on retina of rats with acute ocular hypertension. Methods The SpraqueDawley (SD) rats were randomly divided into the normal group, the model group and PC high or lowdosage group. The PC high or low dose group received 300mg/kg.d or 100mg/kg.d of PC in suspension solution for 5 days respectively. The normal group and the model group fed with distilled water for 5 days. Then acute ocular hypertension was induced in the model group and all PC groups, and after 48h of ocular hypertension the eyeballs were analyzed by electron microscope and UV spectrophotometer to measure the levels of superoxide dismutase(SOD), malonaldehyde (MDA), nitrogen monoxidum (NO), glutamic acid (Glu) and calcium ion(Ca2+). Results PC could raise the activity of SOD and reduced the levels of MDA,NO,Glu and Ca2+ in retina tissue. Electron microscope examination revealed that PC reduced retinal edema and ganglion cell apoptosis. PC also enhanced the SOD activity and suppressed the levels of MDA, NO, Glu and Ca2+. Conclusions PC can protect retina from acute ocular hypertension. The main mechanism might relate to anti-free radical oxidation, antagonizing calcium overloading, reducing toxicity of NO and Glu on the retina.
Objective To observe the effects of minocycline to the viability and apoptosis of ratprime;s retinal neuron cells (RNC) under pressure, and to investigate the neuroprotective mechanisms of minocycline against the RNC damage. Methods Establish a model of ratprime;s RNs under pressure cultured in vitro, the protective effect of minocycline is observed by different methods, including observing the morphology of the cells, evaluating the cellsprime; viability by methyl thiazolyl tetrazolium (MTT) colorimetry assay, and detecting the cellular apoptosis with acridine orange/ethidium bromide (AO/EB) double staining by fluorescence microscopy. Immunocytochemistry was used to detect the expression of iNOS and caspase-3 in the cells. Results Obvious morphology changes of RNC were found in cells under pressure compared with the control; the viability of RNC decreased and cellular apoptosis was found in 53.93% cells. The cellular morphology improved in the cells treated by 20 mu;mol/L minocycline, the cellular viability significantly increased, and the cellular apoptosis was found in 17.29% cells. In addition, the expression of iNOS and caspase3 in the treated cells decreased compared with which in the pressured group. Conclusion Minocycline with a certain concentration can effectively inhibit pressureinduced damage and apoptosis of RNC of rats, and the inhibitory effect on expression of iNOS and capases-3 may be the underlying mechanism.
Objective To analyze the protective effects of heat-shock response on the retinae of the rats after retinal ischemic reperfusion injury.Method Twenty Wistar rats (20 eyes) were divided into 4 groups: intracameral perfusion group (group P), intracameral perfusion after quercetin injection group (group P+Q), intracameral perfusion after heat shock group (group P+H), and in tracameral perfusion after quercetin injection and heat shock group (group P+Q+H ). According to the standard program established by International Society for Clinical Visual Electrophysiology, we recorded the results of the dark-adapted electroretinogram (D-ERG ),oscillatory potentials (OPs),and light-adapted ERG (L-ERG) of the rats with intraocular hypertension after induced by heat shock response. The expressions of HSP 70 of the rats in all groups were observed by Western blotting.Results The expression of HSP 70 of the rats in group P+H was the highest in all groups, but the expressions of HSP70 in group P+Q and P+Q+H were inhibited significantly. The amplitudes of a and b wave of ERG and O2 wave of OPs decreased, and the delitescence of them were delayed significantly in rats after intracameral perfusion. The amplitude of b wave of D-ERG and O2 wave of OPs in group P+H were higher than which in group P. Zero hour after perfusion, the amplitudes of all waves in group P+H increased significantly (Plt;0.05). Twenty-four hours after perfusion, the retinal functional resumption of the rats in group P+H was better than which in group P. In group P+Q and P+Q+H, the delitescences of all waves of ERG and O2 wave of OPs were the longest and the amplitudes were the lowest, and some waves even disappeared.Conclusions The heat-shock response may improve the recovery ability of the retinal cells after injury of ischemic reperfusion.(Chin J Ocul Fundus Dis，2003，19：117-120)
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.
Objective To evaluate the efficacy and safety of latanoprost versus travoprost for primary open-angle glaucoma (OAG) and ocular hypertension (OH). Methods All the randomized controlled trials (RCTs) about treating primary open-angle glaucoma and ocular hypertension with latanoprost and travoprost were collected by searching MEDLINE, EMbase, OVID and CNKI. The assessment of methodological quality and data extraction of the included studies were performed independently by two reviewers, and the meta-analysis was conducted with RevMan 5.0 software. Results A total of 13 RCTs involving 1 433 patients were included. The results of meta-analyses showed that, a) At the second week, travoprost showed greater intraocular pressure (IOP) lowering efficacy compared with latanoprost (WMD= –1.47, 95%CI –2.62 to –0.33). At the first month (WMD= –0.50, 95%CI –1.52 to 0.52) and the sixth month (WMD= –0.12, 95%CI –0.85 to 0.61), the difference of IOP reduction between latanoprost and travoprost group was not significant; and b) The latanoprost-treated group showed fewer reported conjunctival congestion than the travoprost-treated group (OR=0.47, 95%CI 0.35 to 0.63). The difference in adverse events of eye pain (OR=0.55, 95%CI 0.27 to 1.12) and iris or skin depigmentation (OR=1.25, 95%CI 0.53 to 2.92) between latanoprost and travoprost group was not significant. Conclusion Latanoprost and travoprost are comparable in lowering IOP for OAG and OH patients. Latanoprost shows greater ocular tolerability with lower incidence of side effects as conjunctival congestion. This conclusion is not powerful enough in proof due to the medium methodology quality of the included studies, so a large number of high-quality RCTs with large sample are needed for objectively, entirely and precisely evaluating the efficacy.
The occurrence of high intraocular pressure (IOP) after vitrectomy for diabetic retinopathy (DR) is related to many factors, including the type and stage of DR, macular detachment, surgical methods, and the type of ocular tamponade. Early high IOP occurred mainly due to laser photocoagulation, inflammatory response, improper ocular tamponade, residual viscoelastic agents and ciliary body dysfunction. In addition to the above reasons, early-middle stage high IOP is also related to tamponade gas expansion peak, encircling scleral buckle and hyphema. The major reason for middle-stage high IOP is hyphema and silicon oil in anterior chamber. The reasons for late-stage high IOP are glaucoma, silicone oil emulsification, long-term use of glucocorticoid, and iris incision closure. Most high IOP can be controlled by proper treatment such as stopping use of glucocorticoid, anti-glaucoma eye drops and surgeries. But there are still a small number of patients with unexplained refractory high IOP, the mechanism need to be further explored.
ObjectiveTo investigate the effect of erigeron breviscapus (EBHM) on ocular hypertension and the protective effect of retinal ganglion cells (RGCs) in rats by regulating mitogen activated protein kinase (MAPK) signaling pathway.MethodsSixty male Sprague-Dawley rats were divided into control group, model group, low-dose EBHM group (group A), medium-dose EBHM group (group B), and high-dose EBHM group (group C) by random number table method. There were 12 rats in the group, the left eye was used as the experimental eye. The rats of model group, group A, group B, and group C were infused with normal saline through the anterior chamber to construct an acute ocular hypertension model; the control group was given general anesthesia only. Then, 2-30 days after modeling, rats in the control group and model group were given 3 ml of normal saline once a day; rats in group A, group B, and group C were given 0.30, 0.45, and 0.60 g/100 g EBHM by intragastric administration, respectively, 1 time/d. The rat intraocular pressure was measured before modeling and 1, 14, and 30 days after modeling, and the proportion of high intraocular pressure model was measured. Thirty days after modeling, hematoxylin-eosin (HE) staining was used to observe the pathological changes of retinal tissue; immunofluorescence staining was used to detect the changes in the number of RGCs; real-time fluorescent quantitative polymerase chain reaction (RT-qPCR) was used to detect p38 in the retinas of rats in each group. The relative expression of MAPK and Caspase-3 mRNA; western blot was used to detect p38MAPK and phosphorylation in the retina of rats in each group relative expression of phosphorylate-p38MAPK (p-p38MAPK) and Caspase-3 protein. One-way analysis of variance was used for multi-sample comparison, and SNK-q test was used for comparison between two samples.ResultsOne day after modeling, none of the rats in the control group developed acute ocular hypertension, and the other groups were successfully modeled. Compared with the model group, the rates of acute ocular hypertension at 14 days after modeling in groups B and C were lower (χ2=98.701, P＜0.05), and the rates of acute ocular hypertension at 30 days after modeling in groups A, B, and C were 0. There was no statistically significant difference in the rates of acute ocular hypertension between 14 and 30 days after modeling in the A, B, and C groups (P＞0.05). The results of HE staining showed that the structure of the retina in the control group was complete, and the layers were clearly visible; the RGCs count was not abnormal, and the morphology was plump and round. The retina of rats in the model group became thinner; the number of RGCs was greatly reduced, the morphology was vacuolated, and the arrangement was sparse. The retina of rats in groups A, B, and C became thicker, and the number of RGCs increased, and the retina structure in group C was better restored. The results of immunofluorescence staining showed that the RGCs counts of rats in groups A, B, and C were higher than those in the model group, and the difference was statistically significant (F=297.514, P＜0.05); pairwise comparison between groups, group A was lower than that of group B and C Group (q=2.842, 5.263), group B was lower than group C (q=2.457), the difference was statistically significant (P＜0.05). The results of RT-qPCR and Western blot showed that compared with the model group, the relative expression of Caspase-3 mRNA (F=267.912) and protein (F=692.279) and the relative expression of p-p38MAPK protein in the retina of rats in groups A, B and C. The expression level (F=150.061) all decreased, and the difference was statistically significant (P＜0.05); pairwise comparisons between groups showed that Caspase-3 mRNA (q=6.977, 15.642) and protein (q=6.997, 15.642) relative expression levels and p-p38MAPK protein (q=12.443, 24.358) relative expression levels are lower than groups A and B, group B was lower than group A (q=11.678, 12.471, 10.204), the difference was statistical academic significance (P＜0.05).ConclusionsEBHM can significantly reduce intraocular pressure in rats with acute ocular hypertension, increase RGCs counts, and reduce retinal damage. Its regulatory mechanism may be related to the MAPK pathway.