Objective To inverstingate the effect of perfluorohexyloctane(F6H8)to the retina of rabbit eyes. Methods Fifteen vitrectomized New Zealand white rabbits were injectedF6H8(experiment group,12 rabbits ) and BSS(control group,3 rabbits) into vitreous cavity.Slit-lamp biomicroscopy and indirect ophthalmoscopy were performed pre- and postoperatively in all the eyes.Histopathological examination was done after the rabbits were sacrificed at the end of the study. Results A large clear balb was formed after intravitreal injection of theF6H8 in the vitreous was injected and no retinal detachment and cataract were found.The OPL was edematous and then thinned out in 4th week in experimental group.Degenerating cells was found in inner and outer nuclear layers.Cellular vaculoar degeneration was present in TEM. ConclusionF6H8 in vitreous cavity may cause significant side effects on retina,we could not recommend it to be used as an intraocular temponade.
One eye each in 3 groups of 12 pigmented rabbits after bilateral vitrectomy received 0.5mg, 1mg or 2mg triamcinolone acetonide (TA), respectively. The fellow eye received only balance saline solution as control. Ophthalmoscopy and electroretinography were performed during 1 day to 38 days after vitrectomy and drug injection. Light and electronmicroscopic studies were done on the 28th day. The particles of drug were visible on day 28 in all TA-treated eyes. Administration of 0. 5rug and 1mg TA did not result in different changes in ERG b-wave amplitudes compared with those in control eyes(P＞0. 05). There were significant elevations of ERG b-wave in 2mg TA eyes compared to the control eyes(Plt;0.05), Both ligbt and electronmicroscopy of the retina in these groups were almost normal. The results showed no Toxielties in TA treated eye up to 2mg after vitrectomy. This offers the experimental evidence as a baseline for combining TA with vitrectomy to reduce recurrence of proliferative vitreoretinopathy. （Chin J Ocul Fundus Dis,1996,12: 105- 107）
Objective To observe the effects of high concentr at ion glucose on the calcium-activated potassium channel of rabbits′ retinal Müller cells. Methods The rabbits′retinal Müller cells were cultured in vitro under the condition of high concentration glucose, and identified by immunohistochemical staining and transmission electron microscopy. Patch-clamp technique was used to observe the changes of the calcium-activated potassium channel of retinal Müller cells caused by high concentration glucose at different time.Results High concentration glucose could inhibit the calcium-activated potassium channel of cultured retinal Müller cells in a time-dependent manner. Conclusion High concentration glucose may reduce the biological functions of Müller cells by inhibiting calcium-activated potassium channel. (Chin J Ocul Fundus Dis，2003，19：164-167)
Objective To investigate the correlation of ascorbic acid distribution and retinal susceptibility to iron toxicity of the retina.Methods Autoclaved iron particles of 5 mg and 15 mg were implanted into the vitreous cavities of 32 Spragu-Dawley (SD) rats and 9 rabbits, respectively. The retinal sections of rats and rabbits were examined after hemotoxylin-eosin (HE) staining. Apoptos is of rabbits′retinal neurons was investigated by TdT-mediated dUTP-biotin nick-end labeling (TUNEL). Chinoy′s method was used to observe the distribution of as corbic acid in the retinae of the 2 kinds of animals.Results In rats, histological and structural densification was observed only in the photoreceptor cells after implantation of the iron particles. In rabbits, however, histological and structural destruction as well as TUNEL-positive nuclei were observed in all neuronal layers of the retina 3 days after the implantation of the iron particles. Silver granules reduced by ascorbic acid from silver nitrate were observed only in the outer nuclear layer in normal rats retinae, while they were observed evenly throu ghout all layers of rabbits′retinae. Conclusions The suscept ibility of retina to iron toxicity is correlated to the distribution of ascorbic acid in retina. (Chin J Ocul Fundus Dis，2003，19：269-332)
ObjectiveTo investigate the protective effect and mechanism of betaxolol on optic nerves after experimental retinal ischemia-reperfused injury.MethodsRetinal ischemia was induced in SD rats by increasing intraocular pressure through intracameral infusion. Sixty-eight rats were randomly divided into 3 groups: normal control (eight rats), 0.25% betaxolol treatment (thirty rats) and saline control group (thirty rats). The latter two groups were subdivided into group 1 day, 3 and 7 days after reperfusion, respectively, with 10 rats in each group. Betaxolol and normal saline was applied to the right eyes of the rats in the treatment group and to the ones in normal saline control group, respectively. The amplitude of bwave of electron retinograph (ERG) was observed and the histological and ultrastructural changes were detected by light and electron microscopy. The expression of neural nitrogen oxide synthase (nNOS) was detected by immunohistochemistry. The content of malonyldialdehyde (MDA) and the superoxide dismutase (SOD) activity were measured by spectrophotometer.ResultsBegan from the first day after reperfusion, in saline control group, the amplitudes of ERG bwave reduced continuously, the histopathological damages of retina were aggravating, the expression of nNOS increased, MDA level increased and SOD level decreased persistently, which significantly differed from the normal control group （P＜0.01）; in contrast to the saline control group, the amplitudes of bwave of ERG in betaxolol treatment group after reperfusion got right obviously（P＜0.01）, with alleviated histopathological damages, decreased nNOS positive neurons（P＜0.01）, decreased MDA content（P＜0.01）, and increased SOD activity （P＜0.01）, in which no statistical significance of nNOS positive neurons was found between the treatment group and normal control group （P＞0.01）. ConclusionBetaxolol, by reducing intracellular overfreight ofCa2+, inhibiting production of NO and elevating the ability of anti-oxidation in rat retina, can protect retinal neurons from ischemiareperfused injury.(Chin J Ocul Fundus Dis, 2005,21:249-252)
Objective To investigate the retinal toxicity and verify the safe dose of intravitreal injecting fluconazole. Methods Twelve healthy adult white rabbits were divided at random into 6 groups：a normal control group and 5 groups received intravitreal injection of a single dose of fluconazole ranging from 10 to 200 mu;g respectively.Retinal toxicity was examined by ophthalmoscopy, electroretinography, light and transmission electron microscopy (TEM) on the third and fourteenth day after injection. Results The ultrastructures of the retinal tissues of the normal control group and fluconazole 10～150 mu;g groups were normal on the third and fourteen day after injection.The light microscopy and TEM showed that cells of all the retinal layers in the 200 mu;g group revealed apparent degenerative changes on the fourteenth day after injection, and the light microscopic picture showed the vacuolar degeneration of outer segments of photoreceptors, the nuclei in outer nuclear layer drop out into inner segments, the vacuolar degeneration of nerve fiber layer, and the proliferation of pigment epithelium. TEM revealed expansion of paranucl eus space and karyopyknosis of the bipolar cells, the swelling of nerve fibers and disappearance of the synapses in the inner plexiform layer, the vacuolation and disappearance of microvilli of the pigment epithelium cells. Conclusion The safe dose of fluconazole injected intravitreally should be 100～150 mu;g. (Chin J Ocul Fundus Dis，2000，16：139-212)
Objective To investigate the effects of advanced glycation endproducts (AGEs) on proliferation of pericytes of bovine retinal capillary vessels and expression of transforming growth factor beta;(TGF-beta;). Methods The proliferation of pericytes detected by methyl thiazolyl tetrazolium (MTT) colorimetric assay, cellular cycle of pericytes was analyzed by flow cytometry was used to analyze cell, and TGF-beta; protein expression of pericytes was observed by immunofluorescent staining. Results AGEs inhibited the proliferation of pericytes of bovine retinal capillary vessels, stopped the cellular cycle of pericytes in synthesis phase (S phase), increased the number of apoptotic cells obviously (Plt;0.01), and promoted the expression of TGF-beta; proteinof perycytes. Conclusions AGEs may promote the apoptosis of pericytes by inhibiting the proliferation of pericytes to lead the decrease of pericytes number, and may accelerate diabetic retinopathy by promoting the expression of TGF-beta; protein of pericytes. (Chin J Ocul Fundus Dis, 2006, 22: 20-23)
Objective To investigate the effects of gamma;-interferon (IFN-gamma; on the expression of costimulatory molecules B7-1 (CD80) and B7-2 (CD86) and Fas/FasL in human retina. Methods Nine human eyes were obtained from the eye-bank of Zhongshan Ophthalmic Center. Six eyes were used for making retinal wholemounts, and 12 retinal wholemounts from each eye were put into the 24-hole culture board which had 2ml DMEM/F12 culture medium in each hole. The wholemounts were divided into 3 groups whose concentration of IFN-gamma; was 0, 200, and 1000 U/ml respectively. After cultured in 37℃ culture box (95%O 2，5%CO 2) for 24 hours, the expressions of B7-1 (CD80), B7-2 (CD86), and Fas/FasL on these retinal wholemounts were detected by immunohistochemical method. The retinal wholemounts from 3 healthy people were detected by immunohistochemical method as the control. Results Expression of FasL but not B7-1, B7-2 or Fas was found in the control group, while the expression of B7-1, B7-2 and Fas and increased expression of FasL were found after cultured with IFN-gamma;. Conclusion IFN-gamma; may be involved in the occurrence of ocular immune response and induction of apoptosis via the stimulation of expression of costimulatory molecules and Fas/FasL, which plays an important role in the activation of T lymphocytes. (Chin J Ocul Fundus Dis, 2006, 22: 117-119)
Objective To observe the effects on rabbit corneas and retinas after single intravitreal injection of voriconazole at different doses. Methods According to the randomization table, 25 healthy rabbits were randomly divided into control group, and voriconazole 50, 100, 200, and 400 μg groups. Therefore, there were 5 rabbits in each group. The eyes of control group received intravitreal injection of 0.1 ml balanced saline solution, and those treatment groups received 0.1 ml voriconazole injection of corresponding dose. Before the injection and 1, 7, and 14 days after the injection, endothelial cell counts and corneal thicknesses were measured; full-field electroretinogram were performed and b-wave amplitudes in maximal combined reaction (Max-R) were recorded. On 14 days after the injection, histologic structures were observed by light microscope and transmission electron microscope. Results There was no significant difference in endothelial cell counts (F=0.320, 0.291, 0.467, 0.649) and corneal thicknesses (F=0.214, 0.284, 0.360, 0.225) with those of control group at any time points (P > 0.05). Before and 1 day after the injection, b-wave amplitudes of each voriconazole group had no significant difference compared with those of control group (F=0.220, 0.106; P > 0.05). On 7 days after the injection, b-wave amplitudes decreased significantly at doses of 200 μg and 400 μg (P < 0.05). On 14 days after the injection, there was no significant difference between the the amplitude of 200 μg group and that of control group (P > 0.05). However, the amplitude of the 400 μg group decreased continuously and there was still significant difference (P < 0.05). Light microscopy did not reveal any corneal abnormality in both control group and voriconazole groups. The retinas were normal except that of the 400 μg group, which hadathinner and degenerated inner nuclear layer and disordered photoreceptor layer. Under transmission electron microscope, there were no ultrastructure damages of corneas in both control group and voriconazole groups, either. The rabbit retinas of the 50 μg and 200 μg group have normal inner nuclear layer and photoreceptor layer, but degrees of changes in both layers were observed in the eyes of 200 μg and 400 μg group. Conclusions There is no obvious effects on rabbit corneas and retinas after single intravitreal injection of voriconazole at he dose less than or equal 100 μg. There are no obvious effects on rabbit corneas at the dose of 200 μg and 400 μg, while there are damages to the retinas in both functions and histological structures.
ObjectiveTo investigate the effect of triamcinolone acetonide (TA) with different dosage and excipient on retina.MethodsThirty-two purebred New Zealand white rabbits randomly divided into 4 groups underwent intravitreous injection with TA. Group 1:4 mg TA without excipient; group 2:25 mg TA without excipient; group 3:4 mg TA with excipient; group 4:25 mg TA with excipient. Electroretinography (ERG) was performed on each rabbit before intravitreal injection, 1 week, 1 and 2 months after the injection. All the animals were killed and the eyeballs were extirpated 2 months after the injection, and pathological examinations including light and electron microscopy were performed.ResultsNo significant difference was found in the latent period of ERG at the points of time before and after the injection in all the groups, but the amplitudes of ERG waves was lower in groups containing excipient than that before the treatment (Plt; 0.01). The results of light and electron microscopy showed damages of tissue or structures of retina in various degrees in groups containing excipient.ConclusionIntravitreous injection of TA with the dosage of ≤25 mg without excipient does no harm to the retinal configuration and function, and excipient may lead to the change of retinal configuration and function.(Chin J Ocul Fundus Dis, 2005,21:229-232)