缺血预处理对大鼠视网膜缺血再灌注损伤保护作用

目的：探讨缺血预处理是否对视网膜缺血再灌注损伤有保护作用及其机理,方法：利用前房灌注生理盐水形成高眼压的视网膜缺血再灌注损伤的动物模型,视网膜缺血时间为1h分别于缺血前30min、24h或72h对大鼠一只眼5min短暂缺血即预处理,24h或72h后行视网膜电图（ERG）、电镜、光镜、丙二醛（MDA）及热休克蛋白70（HSP70）检测,或者一侧眼行5min假处理,24h后行1h缺血,24h或72h再行上述检测,所有对侧眼不作处理作对照,结果：与假处理相相比,缺血前24、72h进行预处理后的大鼠视网膜光镜、电镜表现损害明显减轻,ERGb波明显恢复（P＜0．01）,MDA含量降低（P＜0．01）,缺血前30min预处理的视网膜表现严重的损害,ERGb波几安全消失,结论：缺血预处理对视网膜缺血再灌注损伤有保护作用,且有一定时限性。     

糖尿病大鼠视网膜氧化应激损伤及葛根素的干预作用

目的研究糖尿病大鼠视网膜氧化应激指标的变化及葛根素对其的干预作用。方法 40只清结级雄性SD大鼠,其中构建糖尿病大鼠模型30只,随机分为糖尿病模型组、葛根素低剂量组和葛根素高剂量组,每组10只;另设一正常对照组(10只鼠)。造模成功后,葛根素低剂量组与葛根素高剂量组分别给予葛根素250mg·kg-1·d-1和500mg·kg-1·d-1,正常对照组与糖尿病模型组每日给予3mL灭菌生理盐水。均经食道灌胃给药,每日1次,连续4周。4周后测定各组鼠血清及视网膜中超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(maleic dialdehyde,MDA)、总抗氧化能力(total antioxidant capability,T-AOC)的变化,免疫组织化学法检测视网膜组织8-羟-2’-脱氧鸟苷(8-hydroxy-2’-deoxyguanosine,8-OHdG)和聚腺苷二磷酸核糖聚合酶[poly(ADP-ribose)polymerase,PARP]活性,Western blot法检测p38MAPK蛋白表达。结果造模后4周,与正常对照组相比,糖尿病模型组大鼠血清与视网膜组织中SOD活性明显下降,分别为(83.20±5.51)U·mL-1、(122.96±10.98)U·mg-1;MDA含量显著增高,分别为(29.58±0.41)μmol·L-1、(8.87±0.49)μmol·g-1;视网膜中T-AOC含量明显下降,为(1.72±0.31)U·mg-1(均为P<0.05)。gn糖尿病模型组相比,葛根素低剂量组血清SOD活性升高,为(97.80±1.75)U·mL-1(P<0.05),但其他指标变化不大(均为P>0.05)。与糖尿病模型组相比,葛根素高剂量组血清与视网膜组织中SOD活性升高,分别为(114.17±4.02)U·mL-1、(146.48±8.04)U·mg-1;视网膜TAOC含量升高,为(2.12±0.37)U·mg-1;血清和视网膜MDA含量降低,分别为(20.73±1.51)μmol·L-1、(5.73±0.76)μmol·g-1(均为P<0.05)。正常对照组大鼠视网膜中8-OHdG、PARP阳性细胞极少,糖尿病模型组表达较正常对照组明显增加,葛根素干预后表达明显减弱,葛根素高剂量组作用更显著。Western blot结果显示:各组大鼠视网膜中总p38MAPK表达无明显差异(P>0.05),但糖尿病模型组视网膜p38MAPK的磷酸化程度较正常对照组显著增强,高剂量葛根素干预后p38MAPK的磷酸化程度明显下降(P<0.05)。结论糖尿病大鼠存在视网膜的氧化应激损伤,葛根素可减轻该损伤作用,其机制可能与p38MAPK信号途径有关。     

The protective effect of ascorbate in retinal light damage of rats

Cyclic light and dark-reared rats were exposed to intense visible light for various periods and then rhodopsin-measured following recovery in darkness for up to 14 days. Animals were injected with ascorbic acid or ascorbate derivatives at various doses prior to light exposure in green Plexiglas chambers. The results show that ascorbic acid administration elevates retinal ascorbate and reduces the loss of rhodopsin and photoreceptor cell nuclei resulting from intense light. When given in comparable doses, L-ascorbic acid, sodium ascorbate, and dehydroascorbate were equally effective in preserving rhodopsin. The ascorbate protective effect in the retina is also dose dependent in both cyclic light and dark-reared rats and exhibits a requirement for the L-stereoisomer of the vitamin. Ascorbic acid is effective when administered before, but not after, light exposure, suggesting that protection from light damage in the retina occurs during the light period. In some experiments, rod outer segments were isolated from rats immediately after light exposure, lipids extracted, and fatty acid composition determined. As judged by the preservation of rod outer segment docosahexaenoic acid in rats given ascorbate, the vitamin may act in an antioxidative fashion by inhibiting oxidation of membrane lipids during intense light.     

Retinal ischemia with neovascularization in cisplatin related retinal toxicity

PURPOSE: To report a case of macular ischemia and retinal neovascularization in a patient who received cisplatin related chemotherapy. DESIGN: Interventional case report. METHODS: A patient with germ cell testicular tumor received polychemotherapy (bleomycin, etoposide, and cisplatin or BEP) for a recurrence of his tumor. Ten weeks after completion of treatment, he presented with loss of vision in his left eye. RESULTS: Fluorescein angiography revealed bilateral retinal ischemia and left retinal neovascularization. Panretinal laser photocoagulation was performed. Unfortunately, his vision did not improve. CONCLUSIONS: Like interferon, cisplatin related chemotherapy could cause considerable ocular morbidity. It can cause marked irreversible visual loss at therapeutic dose, and it is not well recognized. Retinal neovascularization related to cisplatin therapy has not been previously reported. Physicians should be aware and warn patients of the potential ophthalmic side effects of cisplatin related chemotherapy.     

尼莫地平对兔视网膜缺血再灌注损伤保护作用的实验研究

目的　探讨尼莫地平对实验性视网膜缺血再灌注损伤的保护作用及其机理。方法　 72只兔随机分为阴性对照组、模型组、尼莫地平组 ,经前房恒压 ( 110mmHg) ( 1kPa =7.5mmHg)灌注生理盐水 6 0min ,建立视网膜缺血损伤的动物模型。并于造模前 6h及 1h尼莫地平组行尼莫地平溶液灌胃 ,模型组及对照组予等量生理盐水灌胃。观察缺血再灌注损伤后 1、3、7、15d各组视网膜组织学及超微结构变化 ,计数视网膜神经节细胞 (retinalganglioncells,RGC) ,视网膜内层厚度 (thicknessofinnerretinallayers ,TIRL) ,测定丙二醛(malondialdehyde,MDA)、超氧化物歧化酶 (superoxidedismutase,SOD)含量。 结果　模型组再灌注后 1d ,视网膜各层结构即有不同程度的损伤 ,3、7、15d出现节细胞数目减少 ,视网膜内层厚度变薄 ,伴随MDA升高和SOD降低 ,上述变化随时间延长而加重。尼莫地平治疗组RGC和TIRL均从第 3天开始较模型组有显著性增加 ,RGC计数 7d时增加最显著 (P <0 .0 1) ;IRL厚度 15d时增加最显著 (P <0 .0 1)。尼莫地平组各时间点MDA含量均低于模型组 ,而SOD活性都高于模型组 ,差异有显著性。各时间点RGC计数减少和IRL厚度降低呈显著正相关 (r =0 .90 5 ,F =2 7.2 7,P <0 .0 1) ;视网膜MDA含量的降低和SOD活性的升高呈显著     

FK506对糖尿病大鼠视网膜损伤的保护作用初步研究

目的 探讨FK506对糖尿病早期血-视网膜屏障破坏及视网膜神经节细胞的凋亡是否具有保护作用.方法 成年雄性Wistar大鼠,链脲佐菌素(Streptozotocin,STZ)腹腔注射诱导糖尿病,取成模后14 d大鼠选其中一眼玻璃体腔注射FK506 2.5 ng作为FK506玻璃体腔注射组;玻璃体注射对照组取成模后14 d大鼠任选一眼注射等体积的药物溶剂.手术后48 h取材应用免疫荧光技术检测视网膜铺片Occludin的表达改变,TUNEL法检测视网膜神经节细胞凋亡情况.结果 糖尿病大鼠FK506注射组视网膜毛细血管及动脉中Occludin表达呈梭形网状排列,排列紊乱、中断,在胞浆内即网眼中可伴点状染色,玻璃体注射对照组视网膜毛细血管及动脉中荧光强度较弱,网眼的排列更为紊乱,中断现象严重.玻璃体注射对照组视网膜节细胞层见少量的凋亡细胞(9.2±3.4)个/切片,FK506注射眼未发现凋亡细胞,两组比较差异显著有统计学意义.结论 FK506可增加Occludin的表达及维持其正常分布,并可抑制视网膜神经节细胞凋亡,我们认为其对糖尿病引起的视网膜损害有保护作用.     

藏红花素对大鼠视网膜缺血-再灌注损伤的保护作用

目的　观察大鼠视网膜缺血-再灌注损伤（retinal ischemia-reperfusion injury，RIRI）时藏红花素对视网膜细胞凋亡数目、凋亡相关蛋白Caspase-3表达的影响，探讨缺血再灌注时藏红花素对视网膜的保护作用机制。方法　选取体质量200~250 g的健康雄性SD大鼠24只，随机分为4组:对照组、模型组、藏红花素低剂量组和藏红花素高剂量组，每组6只。藏红花素低剂量组、高剂量组分别于造模前3 d、30 min定时腹腔注射5 g·L^-1藏红花素5 mg·kg^-1、50 mg·kg^-1。造模成功后24 h处死大鼠并摘取眼球。使用电镜观察各组大鼠视网膜细胞结构，TUNEL染色检测视网膜凋亡细胞数量，免疫组织化学染色法观察凋亡相关蛋白Caspase-3在视网膜中的表达。结果　视网膜TUNEL染色发现，对照组视网膜组织中几乎未发现凋亡细胞的阳性表达，模型组视网膜神经节细胞层和内核层中发现大量棕黄色着色的细胞，其凋亡细胞数为（27.40±0.96）个，藏红花素低剂量组可见神经节细胞层、内核层凋亡细胞数较模型组减少，凋亡细胞数为（8.40±0.41）个，与模型组相比差异有统计学意义（P<0.01）；藏红花素高剂量组凋亡细胞数较模型组和低剂量组明显减少，凋亡细胞数为（4.30±0.47）个，和藏红花素低剂量组相比差异有统计学意义（P<0.01）。对照组大鼠视网膜组织Caspase-3染色阴性，模型组视网膜神经节细胞层可见棕黄色颗粒位于细胞浆内，藏红花素低剂量组Caspase-3蛋白表达量与模型组类似，藏红花素高剂量组Caspase-3蛋白表达量与对照组类似。结论　藏红花素能通过降低Caspase-3蛋白含量及凋亡细胞数，从而有效保护视网膜免受RIRI。     

Electrophysiological evaluation of the protective effect of dimethylthiourea against retinal photic injury

PURPOSE: The Protective effect of dimethylthiourea (DMTU) against photic injury of the retina was evaluated by electroretinogram (ERG). METHODS: In the DMTU-treated group, 250, 500, or 750 mg/kg DMTU was administered intraperitoneally to albino rabbits at 24 hours and immediately before starting light exposure to the eye. In the control group, physiological saline was injected intraperitoneally instead of DMTU. Preservation rates of ERG a-, b- and c-wave amplitudes were defined as the percentages of the post-photic injury values to the pre-photic injury ones, and were compared between the control and the DMTU-treated groups. RESULTS: In 750 mg/kg DMTU-treated group, the preservation rate of the a-wave was significantly higher than that in the control group 24 hours after the photic injury. While the preservation rate of the c-wave was remarkably low in the control group 24 hours after the photic injury, it was significantly higher in the 500 and 750 mg/kg DMTU-treated groups. Furthermore, better preservation rates of the c-wave were noted with higher doses of DMTU. CONCLUSION: These results suggest that DMTU protects against photic injury of the retinal pigment epithelium and photoreceptors.     

Retinal ischemia and risk of neovascularization following central retinal vein obstruction

The predominant risk factor for the development of neovascular complications involving the retina (NVR), the optic disc (NVD), and iris (NVI) following central retinal vein obstruction (CRVO) is the extent, location, and duration of retinal ischemia (ischemic drive). The extent of retinal capillary nonperfusion (ischemic index) was quantitated by microcomputer analysis of 200 standard fundus-iris fluorescein angiograms. The results were correlated with the development of neovascularization in eyes not receiving prophylactic argon laser panretinal photocoagulation (PRP). Of the 85 eyes with intact capillary perfusion (hyperpermeable group), none developed NVR/NVD and only one eye (1%) developed neovascular glaucoma (NVG). Twenty-nine eyes exhibited moderate degrees of retinal ischemia (indeterminate group), and three eyes (10%) developed NVR/NVD, with two eyes (7%) developing NVG. Of the 86 eyes with extensive retinal capillary nonperfusion (ischemic group), 28 eyes (33%) developed NVR/NVD and NVG occurred in 39 eyes (45%). The inherent difficulties in following high risk patients clinically and angiographically at frequent intervals over extended periods of time, the tendency for rapid progression of early NVI to NVG, and the relatively poor results following treatment in advanced cases make the early recognition of eyes at high risk to develop NVG essential and the initiation of prophylactic PRP as the treatment of choice in this disorder.     

己酮可可碱对大鼠急性高眼压性视网膜缺血再灌注损伤的保护作用

目的:探讨己酮可可碱对大鼠视网膜缺血再灌注损伤的保护作用及机制。方法:视网膜缺血再灌注模型是通过提高前房眼内压来实现的。将35只Wistar大鼠随机分为3组:正常组5只,对照组15只,治疗组15只。治疗组于高眼压前6h和眼压正常后即刻己酮可可碱50mg/kgip,对照组于相同时间点等容量生理盐水ip。监测视网膜电流图(ERG)b波的变化,测定视网膜谷氨酸含量以及视网膜线粒体钙含量。结果:治疗组和对照组谷氨酸含量都在缺血再灌注后逐渐上升,在48h达到峰值,两组都明显高于空白对照组(P<0.01)。在6h点治疗组与对照组间无显著差异,在其他时点对照组的Glu含量明显高于治疗组(P<0.05)。治疗组和对照组视网膜线粒体钙含量在缺血再灌注后逐渐上升,在24h达到峰值,然后逐渐下降。两组都明显高于空白对照组(P<0.01)。在6h点治疗组与对照组间无显著差异,在其他时点对照组的视网膜线粒体钙浓度明显高于治疗组(P<0.05)。再灌注后,对照组ERGb波比较低平;再灌注后1h,对照组、治疗组的ERG相对b波无明显的差异。24h后两组b波都降低到最低,然后逐渐恢复;72h后对照组ERGb波仅恢复到正常眼的69%左右。己酮可可碱处理组ERGb波恢复到正常眼的95%左右,ERGb波明显较对照组高(P<0.01)。结论:己酮可可碱能有效降低视网膜谷氨酸含量及视网膜组织细胞线粒体钙离子含量,促进ERGb波的恢复,缩短了视网膜缺血再灌注的病理过程。对大鼠视网膜缺血再灌注损伤有一定的保护作用。     

重组人促红细胞生成素对大鼠视网膜缺血-再灌注损伤的保护作用

目的 制作Sprague-Dawley (SD)大鼠视网膜缺血-再灌注(RIR)损伤模型,探讨腹腔内注射重组人促红细胞生成素(rHuEPO)对急性RIR损伤所致的大鼠视网膜神经元损伤的保护作用及其对热休克蛋白72(HSP72)表达的影响.方法 采用前房灌注的方式建立RIR损伤模型,灌注压110 mm Hg(1 mm Hg=0.133kPa),缺血时间1h;腹腔注射rHuEPO.78只SD大鼠随机分组:正常组6只,EPO组、EPO+槲皮黄酮组、RIR组各24只,均以右眼为实验眼.采用免疫组织化学法和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)分别测定正常对照组和各实验组大鼠再灌注24h、48 h、72 h和1周视网膜中HSP72及凋亡细胞的表达,观察各组大鼠视网膜病理学改变.结果 ①正常组大鼠视网膜中HSP72表达微弱,各实验组大鼠视网膜中HSP72表达自再灌注12 h开始增强,24h达到高峰,随后逐渐减弱,72 h时表达稍高于正常.再灌注后各时间段,EPO组大鼠视网膜中HSP72表达均高于RIR组、EPO+槲皮黄酮组(P＜0.05).②正常大鼠视网膜中几乎没有凋亡细胞.再灌注后12 h,各实验组大鼠视网膜中可见凋亡细胞,24 h达高峰,48 h后凋亡细胞数逐渐减少;再灌注后各组大鼠视网膜中凋亡细胞数比正常组多(P＜0.05).③再灌注后,RIR组,EPO+槲皮黄酮组大鼠内层视网膜明显水肿,炎性细胞侵入,膜结构逐渐破坏;EPO组大鼠视网膜结构保持相对完整,炎性细胞相对较少.结论 ①HSP72在正常大鼠视网膜中表达微弱,RIR损伤后表达增多.腹腔注射EPO可以明显诱导大鼠视网膜中HSP72的表达增多.②EPO可以减少大鼠RIR损伤后视网膜细胞凋亡,减少视网膜内炎性细胞的浸润,保护视网膜结构,对视网膜具有明显的保护作用.其机制可能与使HSP72表达上调有关.(中国眼耳鼻喉科杂志,2012,12:30-35)     

缺血-再灌注大鼠视网膜TPA变化与视网膜水肿的关系

目的　探讨缺血-再灌注对大鼠视网膜分泌组织型纤溶酶原激活物(TPA)的影响及其与视网膜水肿的关系。方法　采用提高眼压法造成视网膜缺血后,恢复眼压形成血流再灌注。实验分正常对照组、缺血 1h再灌注 1h组、缺血 1h再灌注 2h组、缺血 2h再灌注 1h组和缺血 2h再灌注 2h组。每组各取 10例测试视网膜组织TPA的活性和含水量。结果　缺血-再灌注后,大鼠视网膜组织TPA的活性和含水量随缺血和再灌注时间的延长而升高(P<0 01)。 结论　缺血-再灌注可引起视网膜组织TPA的活性升高和视网膜水肿,是视网膜组织结构和功能损伤的因素之一。     

辅酶Q10对大鼠视网膜光损伤的防护作用研究

目的观察辅酶Q10对实验性大鼠视网膜光损伤的防护作用及其机制。方法30只Sprague-Dawley(SD)大鼠随机分为正常对照组、阳性对照组、辅酶Q10组等3组，用（2000±120）lx绿色荧光灯对SD大鼠进行24 h持续照射，建立视网膜光损伤模型。于光照前24 h、30 min分别通过阳性对照组和辅酶Q10组大鼠尾静脉注射生理盐水和辅酶Q10。光照后第1天常规摘除眼球,光学和电子显微镜观察视网膜组织病理学改变；流式细胞术检测视网膜细胞凋亡率。结果组织病理学检查显示，辅酶Q10组外核层排列整齐，仅见少量凋亡细胞,内、外节轻度水肿，与阳性对照组比较，光损伤后的组织病理改变明显减轻；流式细胞术检测显示，正常对照组视网膜细胞凋亡率为（1.65±1.48）%，阳性对照组为（25.83±2.92）%，辅酶Q10组为（12.43±2.25）%。阳性对照组视网膜细胞凋亡率较正常大鼠视网膜明显升高(t=18.28，P＜0.01),辅酶Q10组的视细胞凋亡率较阳性对照组明显降低（t=9.07，P＜0.01）。结论辅酶Q10对光损伤引起的视网膜损害及视细胞凋亡有较好的防护作用。（中华眼底病杂志，2007，23：122-125）     

Protective effect of TEMPOL derivatives against light-induced retinal damage in rats

PURPOSE: OT-551 (1-hydroxy-4-cyclopropanecarbonyloxy-2,2,6,6-tetramethylpiperidine hydrochloride), a TEMPOL-H (OT-674) derivative, is a new catalytic antioxidant. In the present study, the efficacy of OT-551 and OT-674 in retinal neuroprotection was tested in a model of light-induced photoreceptor degeneration. METHODS: Albino rats were intraperitoneally injected with OT-551, OT-674, or water, approximately 30 minutes before a 6-hour exposure to 2700-lux white fluorescent light. Retinal protection was evaluated histologically by measuring the thickness of the outer nuclear layer (ONL) and functionally by electroretinogram (ERG) analysis, 5 to 7 days after exposure to light. Levels of protein modification by 4-hydroxynonenal (4-HNE) and 4-hydroxyhexenal (4-HHE), which are end products of the nonenzymatic oxidation of n-6 and n-3 polyunsaturated fatty acids, respectively, were measured by Western dot blot analysis immediately after exposure to light. RESULTS: After exposure to light, water-treated animals had a 77% loss of ERG b-wave amplitudes and a 26% and 56% loss of mean ONL thickness in the inferior and superior hemispheres, respectively. Compared with water-treated rats, ERG b-wave amplitudes in light-exposed eyes were significantly higher in 25 (P < 0.05)-, 50 (P < 0.05)-, and 100 (P < 0.001)-mg/kg OT-551-treated rats. Mean ONL thickness in the superior hemisphere was significantly higher in 25 (P < 0.01)-, 50 (P < 0.01)-, and 100 (P < 0.001)-mg/kg OT-551-treated, light-exposed eyes and in 100 mg/kg (P < 0.05) OT-674-treated eyes. No decrease of ONL thickness was observed in the light-protected covered fellow eyes in any animal. Increased levels of 4-HNE- and 4-HHE-protein modifications after exposure to light in water-treated eyes were completely counteracted by 100 mg/kg OT-551. CONCLUSIONS: Systemic administration of OT-551 and OT-674 provides both functional and morphologic photoreceptor cell protection against acute light-induced damage, most likely by inhibiting lipid peroxidation. The protection by OT-551 was greater than OT-674.     

色素上皮衍生因子对大鼠视网膜缺血 再灌注损伤的保护作用

目的已证实色素上皮衍生因子(pigment epithelium-deriv ed factor,PEDF)对中枢神经细胞有抗凋亡作用。本实验评价其对压力诱发的视网膜缺血再灌注的影响。方法经前房灌注维持眼压110 mm Hg (1 mm Hg = 0.133kpa),45 min,建立大鼠视网膜缺血再灌注模型。 随后立即向玻璃体注射10　μ1(0.1μg/μl)PEDF,分别于2d和7d摘除眼球,测量塑 料包埋切片的平均视网膜内层厚度(mean thickness of inner retinal layer,MTIRL) 和视网膜节细胞(retinal ganglion cells,RGC)计数。结果PEDF玻璃体注射7d后治疗组的MTIRL和RGC明显高于对照组[(118.1±5．0) μm对(949±3.0)μm, P<0.05;(6.0±1．0)个/100 μm对(4.5±0.5)个/100 μm, P<0.05]。结论玻璃体内注射PEDF有助于防止视网膜缺血再灌注后神经变性和细胞死亡。(中华眼底病杂志,2001,17:138-140)     

bFGF对光诱导鼠视网膜光感受器细胞变性的保护作用

为探讨ｂＦＧＦ玻璃体腔内注射对光诱导的光感受器细胞变性的保护作用，选用８～１０周的雌性ＳＤ鼠放入１２小时暗、１２小时亮（１４００～１６５０Ｌｕｘ）的氙弧灯循环光下６天，分别于照射前２天或照射的不同时间给动物右眼玻璃体腔内注入生理盐水稀释的ｂＦＧＦ（１μｇ／１０μｌ）２０μｌ，左眼注入等量的生理盐水。光照后１０天，生理盐水注射眼绝大多数的外核层细胞及光感受器内外段丧失；而光照前及光照早期给药眼，外核层细胞及光感受器的内外段明显厚于对侧眼。初步研究结果表明，早期玻璃体腔内应用ｂＦＧＦ对光诱导的鼠光感受器细胞变性有保护作用     

The inhibitory effect of nilvadipine on calcium channels in retinal ganglion cells in goldfish.

PURPOSE: Our aim was to examine the inhibitory effect of nilvadipine on voltage-gated calcium (Ca) channels in solitary ganglion cells. METHODS: Eyes were excised from goldfish. Ganglion cells were enzymatically dissociated from isolated retina. Whole-cell currents were recorded with the perforated-patch clamp technique. RESULTS: Depolarizing step pulses to more than -48 mV evoked a slowly inactivating inward Ca current. The current-voltage relation for the nilvadipine-sensitive current was bellshaped, and the peak current reached a maximum at -8 mV in the presence and absence of nilvadipine. Nilvadipine block of voltage-gated Ca current was dose-dependent between 1 and 100 microM. The half-maximum inhibitory dose was 35 microM. CONCLUSIONS: The inhibitory effect of orally administered nilvadipine on Ca channels had a mild influence in ganglion cells.