Objective To further investigate pathologic mechanism of retinal phototrauma. Methods Twenty Wistar rats were divided into control and experimental groups.Their eyes were extracted in 12，24 and 36 hours after light exposure.HE stained retina samples were examined and TDT-mediated dUTP nick end labelling(TUNEL)method was employed to distinguish apoptotic cells. Results After 12-hour light exposure,slight vesiculation was observed in the rod outer segment of the retinas.After 24-hour light exposure,the outer nuclear layer showed predominant fractured and condensed nuclei and fragmented DNA.After 36-hour light exposure,the rod outer and inner segments were lysed and most of the nuclei in the outer nuclear layer were disappeared. Conclusions Apoptosis of photoreceptor cell is one of the important mechanisms which cause experimental retinal photoinjury of rats. (Chin J Ocul Fundus Dis, 1999, 15: 167-169)
Objective To evaluate the visual results,surgical tec hnique and safety of secondary intraocular lens (IOL) implantation in aphakic eyes following vitrectomy and lensectomy for complicated ocular trauma or retinal detachment． Methods The clinical records of 3 2 cases (32 eyes),received these surgeries during November 1996 and December 1999,were reviewed retrospectively.During the secondary operation，intraocular infu sion through the pars plana was performend and the type of IOL was chosen based on the integrity of lens capsule. Results The study included 30 eyes suffering from trauma (foreign bodies in 15 eyes,penetrating injury with traumatic endophthalmitis and with vitreous hemorrhage in 6 eyes respectively, blunt trauma with lens dislocation in 3 eyes),and 2 eyes with primary retinal detachment.Those eyes all received vitrectomy,lensectomy,and/or remova l of foreign bodies and corneal suture.The interval of two operations ranged from 1 to 16 months with an average of 6.8plusmn;3.7 months.Posterior chamber IOL was implanted in the ciliary sulcus in 25 eyes with a whole or 2/3 of lens capsule,trans scleral suture fixation of IOL in 5 eyes,anterior chamber IOL and IOL with artificialiris in one eye respectively.Silicone oil was removed in 5 eyes duri ng the secondary operation.Post-operative visual improvement was achieved in 29 eyes.Main complications were corneal edema and low intraocular pressure after operation. Conclusion Intraocular infusion and proper IOL implantation during the secondary operation following vitrectomy can provide selected aphakic eyes with better visual recovery. (Chin J Ocul Fundus Dis, 2001,17:96-98)
Objective To investigate the degenerative changes in the inner rat retina after photic injury.Methods After 24 hour-dark adaptation, sixty Lewis rats were exposed in a ventilated green plexiglass chamber that transmitted continuous green light between 480-520 nm with an intensity of 900～1 000 lx. After 24 hour exposure, the rats stayed in darkness and were sacrificed after 1 day, 3,7 or 14 days. The neurons in the inner retina were marked by immunohisto chemical technique and observed by light and electronic microscope.Results The apoptotic photoreceptor cells were noted after photic injury. The degeneration and decreasing number of rod bipolar cells were found after 3 days; the edema of horizontal cells occurred after 1 day but ameliorated gradually; decreasing number of amacrine cells was found after 1 day; sustained edema of ganglion cells and prolifeeration of the Müller cells were found after photic injury. Pyknotic and edematous neruronal degenerations of inner retina were found in ultrastructural study.Conclusion The neurons in the inner retina as well as Müller cells are involved in the degeneration after photic injury. Different neurons manifest different patterns of degeneration.(Chin J Ocul Fundus Dis，2003，19：201-268)
ObjectiveTo observe the early ultrastructural changes of the optic nerves after the brain impact injury.MethodsEighteen 15-week-old Wistar rats were used in the air-pressure brain impact injury examination. All of the rats underwent the procedures of right-parietal-bone fenestration after abdominal cavity anesthesia with 1% sodium pentolbarbital (45 mg/kg), and then they were divided randomly into 3 groups, i.e., mild injury group (8 rats) underwent with 7 kg of air pressure in distance of 11 cm; severe injury group (8 rats) with 7 kg of airpressure in distance of 8 cm; and control group (2 rats) underwent with the parietalbone fenestration but without impact injury.The ultrastructural changes of the optic nerves were observed 1, 6, 24, and 72 hours after the injury by electron microscopy.ResultsThe difference of ultrastructural changes of optic nerve was not obvious in wild injury group and the control group, and the lanthanum nitrate was only found in the blood vessels in optic nerve. The lanthanum nitrate entered the nerve stroma 1 hour after severe and increased as time goes on. Simultaneously, displayed dilatation of endoplasmic reticulum, cavitation and tumefaction of mitochondrion, vacuolation of nerve stroma, and vacuolation of some axis-cylinder were seen in the glial cells.ConclusionThe brain impact injury may cause ultrastructural changes of the optic nerve and increase of permeability of blood vessels. (Chin J Ocul Fundus Dis, 2005,21:41-43)
The opportunity of vitrectomy for opening eyeball injury is one of the important factors affecting the prognosis. Anterior segment wound repaired by routine suturing needs following and continuous treatment with vitrectomy. The key technique of the following treatment should be the debridement of the inside of wound and expurgation of the surrounding tissues adjacent to the wound, and the emphasis should be put on retinal reattchment and stable repairment.
ObjectiveTo investigate the effect of blue light on Ca2+-protein kinase C (PKC) signaling pathway in human retinal pigment epithelial (RPE) cells in vitro. MethodsPrimary human RPE cells were cultured in vitro and characterized. The experiments were carried out using the 4th generation of human RPE cells. The PKC protein level was measured by Western blot to determine the most appropriate concentration of phorbol ester (PMA) and calcium phosphate binding protein (calphostin C) on PKC expression. Non-radioactive isotope method was used to determine the effect of blue light on PKC expression of cultured cells. Blue-light damage model of human RPE cells was established by 6 hour irradiation of medical blue-light lamp [20 W, 450-500 nm wavelength, (2000±500) Lux], and 24 hours prolongation of post-exposure culture. The human RPE cells were randomly divided into 5 groups. Group A did not receive light irradiation, group B only received blue light irradiation, group C was blue light irradiation and 0.1 mmol/L nifedipine treatment, group D was blue light irradiation and 100.0 nmol/L calphostin C treatment, group E was blue light irradiation and 100.0 nmol/L PMA treatment. Intracellular Ca2+ concentration was measured by acetoxymethyl ester (Fluo 3-AM) labelling and confocal microscope imaging. ResultsThe PKC protein expression in 100.0 nmol/L or 200.0 nmol/L PMA-treated groups was higher than 0.1, 1.0, 10.0, and 50.0 nmol/L PMA-treated groups, the difference was statistically significant (F=217.537, P<0.05), but there was no statistically difference between 100.0 nmol/L and 200.0 nmol/L PMA-treated groups (P=0.072). The PKC protein expression in 100.0 nmol/L or 200.0 nmol/L calphostin C-treated groups was lower than 5.0, 25.0, 50.0, and 75.0 nmol/L calphostin C-treated groups, the difference was statistically significant (F=164.543, P<0.05), but there was no statistically difference between 100.0 nmol/L and 200.0 nmol/L calphostin C-treated groups (P=0.385). PKC level in blue light group was higher than non-light group, the difference was statistically significant (t=-9.869, P<0.05). The Ca2+ fluorescence intensity values in group B, C, D and E was higher than group A, the difference was statistically significant (F=26 764.92,P<0.05). The Ca2+ fluorescence intensity values in group E was higher than group B, C and D (P<0.05), and that in group B was higher than group C and D (P<0.05). ConclusionsThe PKC activity and intracellular Ca2+ concentration in human RPE cells increase after blue-light irradiation. Both calcium channel inhibitor nifedipine and PKC inhibitor calphostin C can reduce intracellular Ca2+ concentration in human RPE cells. PMA can induce intracellular Ca2+ concentration in human RPE cells after blue light irradiation.
Open-globe injuries (OGI) result in complicated and diverse conditions with different mechanisms and anatomical locations, which lead to completely different outcomes based on when to perform pars plana vitrectomy (PPV) after trauma. The PPV operation time points are generally divided into early (0 - 3 days), delayed (4 - 14 days), and late (> 2 weeks). There are still some controversies about the PPV time points after OGI. Injuries with intraocular foreign bodies or high risk of infection usually need early surgery to reduce the occurrence of endophthalmitis. However corneal edema and vitreous hemorrhage can increase the difficulties for early diagnosis and surgery. If there is choroidal hemorrhage or severe trauma in the back part of the eye, delayed intervention can allow the blood clots to be liquefied and removed easily. But there is higher incidence of postoperative complications. Late surgery can reduce the difficulty of PPV, but the increased incidence of proliferative vitreoretinopathy may lead to severe retinal traction, tears and postoperative scar formation.
Objective To observe the effect of blue light on apoptosis of cultured human retinal pigment epithelial (RPE) cells in vitro. Methods Human RPE cells were exposed to blue light, and the cells were divided into 3 groups: group A, with various intensity of illumination; group B: with same intensity but different time of illumination; group C: with same intensity and time of illumination but different finish time of the culture. The apoptosis of RPE cells was observed by TdT-dUTP terminal nick-end labeling (TUNEL) and annexin V-fluoresein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry, and transmission electron microscopy. Results The positive cells stained by TUNEL shrinked and turned round, whose nuclei concentrated and congregated like the crescent or hat. Cracked nuclei and membrane bleb were found. Swollen mitochondrial, disappeared inner limiting membrane of mitochondria, and dilation of the rough endoplasmic reticulum with metabolite were observed by transmission electronmicroscopy. In group A, mild damage of RPE cells was found when the threshold value of the intensity of illumination was less than（500±100）lx, and the apoptosis and necrosis of RPE cells aggravated as the intensity of illumination increased; in group B, as the time of illumination extended, the number of apoptotic RPE cells didn′t increase while the necrosis increased; in group C, 6 and 12 hours after illumination, apoptosis of cells was the main injury, while apoptosis with necrosis was found and necrotic cells increased as the time of illumination was prolonged. Conclusions Illumination with blue light may cause damages of human RPE cells in vitro, with the modalities of apoptosis, apoptotic necrosis and necrosis. The extent of injury is dependent on intensity and duration of the illumination. (Chin J Ocul Fundus Dis, 2005, 21: 384-387)
Objective To investigate the causes of failure of the primary vitrectomy,sum up the experience for secondary vitreous surgery and improve the success rate of primary vitrectomy for complicated retinal detachment． Methods The records of a consecutive series of 60 patients(65 eyes)that underwent secondary vitreous surgery between 1997 to 1998 were retrospectively reviewed.The age of patient ranged from 9 to 63 years(mean 36),and the followup period ranged from 3 to 18 months(mean 10.5 months). Results The main causes of failure of the primary vitrectomy were postoperative recurrence of proliferative vitreoretinopathy(PVR),unwell closed retinal breaks,and intra-and postoperative complications.In 46 of 65 eyes the retina was reattached after secondary vitreous surgery(70．1%)．Postoperatively,31 eyes (47.7%) had a visual acuity(VA)improved,16 eyes(24.6%)had a VA unchanged,and 18eyes(27.7%)had a VA reduced．Fifteen eyes(23.1%)had a VA of ge;0.05 and the best VA was 0.4．Thirty-nine eyes were followed-up from 3 to 18 months(mean 10.5)．In 35 of 39 eyes,the retina was reattached(89.7%),26 eyes(40%)had a VA of ge;0.05,and 7 eyes(10.7%)were hypotonic. Conclusions The keys to the success of secondary vitreous surgery are to restore the mobility for retina by eliminating the PVR completely,and avoid intraoperative complicattions by choosing the appropriate closure procedure for retinal breaks and the suitable intraocular tamponades. (Chin J Ocul Fundus Dis,20000,16:24-26)
Purpose To evaluate the efficacy of vitreous surgery for treatment of fundus damages caused by ocular blunt trauma. Methods Clinical records were reviewed retrospectively for a series of consecutive 101 patients (105 eyes) with fundus damages caused by ocular blunt trauma underwent vitreous surgery from October 1992 to March 1998． Results Based on clinical examination and findings during surgery,all cases were divided into 4 subgroups:vitreous hemorrhage(VH)in 23 yes,VH with retinochoroidal rupture or optic damage in 25 eyes,traumatic retinal detachment in 46 eyes,and retinal giant tear in 11 eyes.Vision acuity improvement achieved in 77 eyes(73.3%)and of them 69 eyes(65．7%)had 0.02～0．6with 38 eyes(55．0%)better than 0．1.Two eye s with no light perception obtained better than 0.1． Visual acuity remained unchanged in 26 eyes(24.8%)and 2 eyes(1.9%)became worse after operation．The retina reattached in 54 eyes(94.7%). Conclusion Severe ocular blunt trauma may cause visual impairment and various fundus damages.Appropriate vitreous surgery can salvage most eyes with those injuries. (Chin J Ocul Fundus Dis,1999,15:100-102)