大鼠慢性高眼压诱导视神经损伤的研究

目的建立大鼠慢性高眼压模型,对其眼压、视网膜节细胞(RGCs)和视神经轴突损伤进行研究。方法对40只大鼠行慢性高眼压模型手术,分为4组:术后即刻、5 d、2周和4周,每组10只,分别测定眼压。采用全视网膜-RGCs Cresyl Violet染色,术后2周和4周对大鼠视网膜进行RGCs计数,并对视神经进行对位苯二胺(PPD)染色。对照组20只大鼠,分为2组,每组10只。结果31只大鼠眼压升高,眼压升高率为77.5%,且4周内眼压维持稳定。眼压升高2周时中心和周边RGCs分别减少11.0%和11.3%,眼压升高4周时中心和周边视网膜分别丢失RGCs达17%和24.6%,与正常对照组比较差异均有统计学意义(P<0.05);而眼压未升高的RGCs未见明显丢失,与正常对照组相比差异无统计学意义(P>0.05)。高眼压组大鼠视神经轴突在颞上方有大约5.3%损伤,球后1 mm的视神经在光镜下可以看到视神经轴突水肿和髓鞘碎屑。结论慢性高眼压动物模型是一种可以重复且有效的青光眼模型,它模拟了人类慢性眼压升高所导致的RGCs丢失和视神经的损伤。     

肝细胞生长因子在原发性开角型青光眼视神经损伤中的作用及机制研究

目的 探讨肝细胞生长因子( HGF)的受体间质表皮转化因子(c-met)激活是否能促进视网膜神经节细胞存活和再生,以及HGF在慢性青光眼大鼠模型中可能的神经保护作用机制.方法 SD大鼠随机分成3组:正常对照组、慢性高眼压组、慢性高眼压HGF注射组;灼烧3条巩膜上静脉制备慢性青光眼模型;烧灼巩膜上静脉术后立即在玻璃腔内注射4 μl HGF(1 μg/μl);iCare眼压计检查大鼠的眼内压变化;ELISA法测定前房内HGF水平;免疫染色检查c-met在视网膜细胞中的分布;使用末端脱氧核苷酸转移酶dUTP缺口末端标记( TUNEL)染色观察视网膜神经节细胞的凋亡;Western blot法检测蛋白激酶B(Akt)、磷酸化蛋白激酶B( p-Akt)、B细胞淋巴瘤基因-2(Bcl-2)和抗凋亡蛋白B细胞淋巴瘤/白血病-xl(Bcl-xl)蛋白的表达水平.结果 术后早期眼压显著升高,并维持2周;与正常组相比,慢性高眼压大鼠组前房HGF明显升高;与慢性高眼压组相比,慢性高眼压注射HGF组TUNEL标记的RGC减少,差异有统计学意义( P＜0. 05);在视网膜中,c-met主要在神经节细胞(RGC)层的细胞中表达;在视网膜样本中,与正常对照组比较,慢性高眼压组p-Akt、Bcl-2和Bcl-xl蛋白表达显著下调(P＜0. 05);与慢 性高眼压组相比,慢性高眼压 HGF 注射组 p-Akt、Bcl-2 和Bcl-xl蛋白表达显著上调(P＜0. 05).结论 HGF可能通过激活Akt信号通路以及增加其下游的相关抗凋亡蛋白表达而发挥对慢性高眼压视神经的保护作用.     

Enhanced protein expression of proBDNF and proNGF in elevated introcular pressure-induced rat retinal ischemia

Purpose Our previous study has shown that expression of p75NTR and sortilin was increased in ischemic retina induced by elevated intraocular pressure (IOP). In this study, we aimed to ascertain the protein expression changes of proNGF and proBDNF in the same situation, since both of them can interact with sortilin and p75NTR. Methods First, expression of proBDNF and proNGF was characterized in normal rat retina by double-labeling immunochemistry. Then, proBDNF and proNGF expression in rat retina with elevated IOP and retinal ischemia was examined by Western blotting and analyzed by statistical methods. Results Immunocytochemistry showed that the proBDNF expressed in the ganglion cell layer (GCL) of normal rat retina while the proNGF primarily existsed in both the nerve fiber layers (NFL) and large ganglion cell bodies. Western blotting analysis demonstrated molecule weights of 32KDa and 28 (proBDNF) /25KDa (proNGF). In case of elevated IOP-induced retinal ischemia, the 28/25KDa band was increased significantly (p<0.05) while the 32KDa band showed little change at day 3, 5 and 7. Conclusion These results suggested that proBDNF protein expressed in the GCL and proNGF primarily presented in NFL and large ganglion cell bodies of normal rat retina and the protein expression forms of 28KDa proBDNF and 25KDa proNGF increased in ischemic retina induced by elevated IOP.     

大鼠视网膜缺血再灌注后多聚二磷酸腺苷核糖聚合酶的表达变化

目的观察大鼠视网膜缺血再灌注损伤后不同时相视网膜结构变化及多聚二磷酸腺苷核糖聚合酶(PARP)的表达情况。方法升高眼压到110mmHg持续1h，建立大鼠视网膜缺血再灌注模型。HE染色观察视网膜组织病理学改变；免疫组化Ehvision^TM法检测视网膜细胞PARP表达。结果正常对照组大鼠视网膜仅见微量PARP表达；缺血1h再灌0h组视网膜结构未见明显变化；再灌注6h，视网膜开始有中性粒细胞浸润，神经节细胞层(ganglion cell layer，GCL)PARP表达显著增加；12、24h组视网膜中有较多中性粒细胞浸润，神经节细胞层PARP表达24h达高峰后下降，但仍维持较高水平；24h后内核层(inner nuclear layer，INL)细胞PARP表达明显增高，168h达高峰，伴之神经节细胞层和内核层细胞明显变薄。另外，也见自身对照眼视网膜神经节细胞层PARP表达增加。结论大鼠视网膜缺血再灌注早期PARP即表达上调，24h组在GCL达高峰，168h组在INL达高峰，这一过程可能与视网膜神经节细胞层和内核层细胞凋亡有关。     

杞菊地黄丸对青光眼模型大鼠视网膜结构的保护作用及其机制

目的：探讨杞菊地黄丸对青光眼大鼠模型视网膜结构的保护作用,并阐明其作用机制。方法：50只SD大鼠随机分为空白对照组,模型组,低、中和高剂量杞菊地黄丸组（n=10）;除空白对照组外各组大鼠通过烙闭大鼠巩膜上静脉制作青光眼动物模型,低、中和高剂量杞菊地黄丸组大鼠分别灌胃给予剂量为1、2和4 g·kg^-1的杞菊地黄丸,空白对照组和模型组大鼠分别灌胃给予等体积生理盐水,每天1次。12周后处死大鼠,取眼球制石蜡切片,行HE染色;TUNEL染色检测视网膜神经节细胞的凋亡情况,采用实时荧光定量PCR（RT-PCR）检测各组大鼠视网膜组织中B淋巴细胞瘤2（Bcl-2）、Bcl-2相关X蛋白（Bax）和含半胱氨酸的天冬氨酸蛋白水解酶3（caspase-3）mRNA表达水平,采用免疫组织化学法检测各组大鼠视网膜组织中Bcl-2、Bax和caspase-3蛋白表达水平。结果：与空白对照组比较,模型组大鼠视网膜神经纤维排列不整齐,纤维间质水肿,细胞层呈空泡样,视网膜神经节细胞数目明显减少;与模型组比较,高剂量杞菊地黄丸组大鼠眼视网膜神经节细胞数目增多,低和中剂量杞菊地黄丸组大鼠眼视网膜神经纤维细胞排列整齐且神经节细胞形态正常。与模型组比较,低、中和高剂量杞菊地黄丸组大鼠视网膜神经节细胞凋亡指数明显减少（P<0.05）,Bcl-2 mRNA及蛋白表达水平明显升高（P<0.05）,Bax和caspase-3 mRNA及蛋白表达水平明显降低（P<0.05）。结论：杞菊地黄丸通过调控Bcl-2、Bax和caspase-3 mRNA和蛋白的表达,抑制视网膜神经节细胞的凋亡,对青光眼大鼠视网膜起保护作用。     

大鼠慢性高眼压视网膜损害相关基因表达谱的研究

目的研究大鼠激光慢性高眼压视网膜损害相关基因表达谱的改变。方法采用5705点的大鼠高密度Oligo基因芯片，对运用532-二极管激光建立大鼠高眼压模型视网膜的基因表达情况进行检测，以对侧眼作为对照。结果通过筛选基因表达谱，得到5277条在大鼠视网膜中有表达的基因，然后采用两两对比组合，从中筛选出了11条差异在2倍以上的基因，其中3奈上调，8条下调。结论在大鼠高眼压模型视网膜中筛选到了11条表达差异〉2倍的基因，可望为青光眼的神经损伤机制及治疗提供新的思路。     

Enhanced expression of proneurotrophins in elevated introcular pressure-induced rat retinal ischemia

Background  Proneurotrophins such as the precursor of nerve growth factor (proNGF) and the precursor of brain-derived neurotrophic factor (proBDNF) interacted with sortilin and p75^NTR to form a complex capable of activating an apoptotic signaling. We found that the expression of p75^NTR and sortilin was increased in ischemic retina induced by elevated intraocular pressure (IOP), but the protein expression changes of proNGF and proBDNF in the same situation were not clear. This study aimed to ascertain the protein expression changes of proNGF and proBDNF in ischemic retina induced by elevated IOP.

Methods  Expression of proBDNF and proNGF was examined by double-labeling immunochemistry in normal rat retina, examined using Western blotting and analyzed using statistical methods in ischemic retina induced by elevated IOP.

Results  Immunocytochemistry showed that the proBDNF expressed in the ganglion cell layer (GCL) while the proNGF primarily existsed in both the nerve fiber layers (NFL) and large ganglion cell bodies of normal rat retina. Western blotting analysis demonstrated that the molecule weights of 28 kD (proBDNF) / 25 kD (proNGF) band were increased significantly (P <0.05) at days 3, 5 and 7 after retinal elevated-IOP-induced ischemia.

Conclusion  ProBDNF expressed in the GCL and proNGF primarily presented in NFL and large ganglion cell bodies of normal rat retina, the protein expression forms of 28 kD proBDNF and 25 kD proNGF increased in ischemic retina induced by elevated IOP.

     

The effect of melatonin on retinal ganglion cell survival in ischemic retina

Our objective was to determine whether melatonin increases retinal ganglion cell (RGC) survival in ischemic mouse retina. Transient retinal ischemia was induced by an acute elevation of intraocular pressure in C57BL/6 mice. To evaluate the effect of melatonin on retinal ischemia, an equal amount of either melatonin or vehicle was intraperitoneally injected into the mice 1 hour before ischemia, at the time of ischemia, and 1 hour after ischemia. Hypoxia inducible factor 1α (HIF-1α) and glial fibrillary acidic protein (GFAP) expression were assessed 6, 12, and 24 hours after ischemia-reperfusion by Western blot. RGC survival was measured 2 weeks after ischemia-reperfusion. The expression of HIF-1α and GFAP peaked 24 hours after ischemia-reperfusion in ischemic retina. The treatment of ischemic retina with melatonin resulted in the inhibition of increased expression of HIF-1α and GFAP. RGC survival was greater in retinas treated with melatonin than in retinas treated with vehicle 2 weeks after ischemia-reperfusion. On the basis of our results, we suggest that melatonin treatment increased RGC survival in ischemic mouse retina. The neuroprotective effect of melatonin is mediated by the inhibition of HIF-1α stabilization and reduced activity of glial cells in ischemic mouse retina.     

大鼠慢性高眼压模型视网膜神经节细胞谷氨酸受体2表达的研究

目的探讨青光眼视网膜神经节细胞（RGC）选择性损伤机制。方法用结扎上巩膜静脉联合术后球结膜下注射5一氟尿嘧啶的方法建立大鼠慢性高眼压模型。模型建立后1周、1个月,在视网膜铺片上行免疫组织化学染色,在激光共聚焦显微镜下观察视网膜谷氨酸受体（GluR）2以及神经丝蛋白（NF）-68的表达情况。结果结扎上巩膜静脉联合术后球结膜下注射5-氟尿嘧啶可诱导较长时间稳定高眼压,1个月内12只高眼压眼眼压均大于22mmHg（1mmHg=0．133kPa）。在正常对照组及高眼压组,大、中、小直径的RGC均可表达NF-68,但NF-68在大直径的神经节细胞的表达更为明显。在正常对照组,大鼠大RGC均缺乏GluR2的表达,而中、小直径RGC大都可表达GluR2;高眼压1周以及1个月组,中、小直径RGCGluR2的表达没有明显变化;高眼压1周,NF-68阳性的大直径的RGC仍缺乏GluR2的表达;但到高眼压1个月,残存NF-68阳性的大直径的RGC开始表达GluR2。结论大RGC对高眼压的易损性可能与其特异性缺乏GluR2表达有关。     

当归多糖对青光眼大鼠视网膜神经细胞的保护作用及其机制

目的：探讨当归多糖对青光眼致大鼠视网膜神经细胞损伤的保护作用,并阐明其机制。方法：将84只SD大鼠随机分为对照组、模型组、阳性药组、低剂量当归多糖组、中剂量当归多糖组和高剂量当归多糖组,每组14只,采用烧灼烙闭巩膜上静脉法建立大鼠青光眼模型。检测各组大鼠眼压值;采用比色法测定大鼠视网膜组织中超氧化物歧化酶（SOD）活性及丙二醛（MDA）和一氧化氮（NO）水平;采用RT-PCR法和Western blotting法检测大鼠视网膜组织中Caspase-3 mRNA和蛋白表达水平。结果：与对照组比较,模型组大鼠各时间点眼压明显升高（P<0.05）;与模型组比较,不同剂量当归多糖组大鼠眼压明显降低（P<0.05）;与低剂量当归多糖组比较,高剂量当归多糖组大鼠眼压明显降低（P<0.05）。比色法测定,与对照组比较,模型组大鼠视网膜组织中SOD活性明显降低（P<0.05）,MDA和NO水平明显升高（P<0.05）;与模型组比较,不同剂量当归多糖组大鼠视网膜组织中SOD活性明显升高（P<0.05）,MDA和NO水平均明显降低（P<0.05）;与低剂量当归多糖组比较,高剂量当归多糖组大鼠上述指标差异均有统计学意义（P<0.05）。RT-PCR和Western blotting法检测,与模型组比较,不同剂量当归多糖组大鼠视网膜组织中Caspase-3 mRNA和蛋白表达水平明显降低（P<0.05）;与低剂量当归多糖组比较,高剂量当归多糖组大鼠视网膜组织中Caspase-3 mRNA和蛋白表达水平明显降低（P<0.05）。结论：当归多糖对青光眼模型大鼠的视网膜组织有保护作用,可以降低视网膜组织MDA和NO水平,升高SOD活性,同时降低视网膜组织中Caspase-3 mRNA和蛋白表达水平,这可能是当归多糖保护视网膜组织神经细胞的机制之一。     

Bcl-2、Bax在慢性高眼压大鼠视网膜的表达

目的探讨Bcl-2、Bax在慢性高眼压大鼠视网膜的表达,以及与慢性高眼压大鼠视网膜损伤的关系。方法健康成年SD大鼠20只,分为正常组和实验组,每组各10只。实验组烙闭大鼠巩膜上静脉制作慢性高眼压模型,造模2个月后,通过HE染色观察视网膜神经节细胞丢失情况,用免疫组织化学法检测视网膜中Bcl-2、bax的表达。结果光镜下观察实验组较正常组神经节细胞数量减少（P〈0.05）。Bcl-2蛋白在正常组及实验组大鼠视网膜上均有阳性表达,位于神经节细胞层及内核层,实验组较正常组Bcl-2表达程度有增高,差异有统计学意义（P〈0.05）。正常组大鼠视网膜中Bax蛋白在神经节细胞层有弱阳性表达,实验组Bax蛋白表达位于神经节细胞层和内核层,表达程度明显增强,与正常组比较差异有统计学意义（P〈0.05）。结论 Bcl-2及Bax的表达失衡可能是慢性高眼压视网膜神经节细胞凋亡的原因之一。     

A new rat model of glaucoma induced by intracameral injection of silicone oil and electrocoagulation of limbal vessels

Background  A satisfied glaucoma model is absent now. The aim of this study was to evaluate the effect of a combination of intracameral injection of silicone oil and electrocoagulation of corneal limbal vessels and episcleral veins in the rats to establish glaucoma model.

Methods  Operation was performed in each of the left eyes of 90 adult male rats. Right eyes were used as controls. Measurement of intraocular pressure (IOP) was performed with an applanation tonometer (Tono-Pen). Retinal ganglion cells (RGCs) were retrogradely labeled by applying FluoroGold onto the bilateral superior colliculus.

Results  During the follow-up (24 weeks), the IOP of the study eyes was significantly higher (P <0.05) than the control eyes (at final examination, IOP of control eyes was (13.4±1.0) mmHg and IOP of study eyes was (16.1±1.8) mmHg). Correspondingly, at 24 weeks after operation, the RGCs density of the study eyes (2286.11±290.45/mm²) was significantly lower than the control eyes (2626.46±164.85/mm², P <0.01). In the operated eyes, histological examination showed excavation of optic disc and increased neuroglial cells in the optic nerve, reduced thickness of retina and diminution of retinal ganglion cells, and atrophy of ciliary body and iris. Notably, the anterior chamber angle of the operated eye remained open.

Conclusions  A combination of intracameral injection of silicone oil and electrocoagulation of corneal limbal vessels and episcleral veins may establish a reliable glaucoma model for further research.

     

睫状神经营养因子与视网膜神经节细胞

睫状神经营养因子作为神经营养因子家族中的重要成员,广泛分布于中枢神经系统。视神经与视网膜是中枢神经系统的一部分。视网膜神经节细胞在视觉通路中起着重要的传导作用。睫状神经营养因子作为一种非靶源性神经营养因子,在视网膜神经节细胞的生长发育过程中,起着重要的调控作用;同时睫状神经营养因子对于损伤的视网膜神经节细胞有促进其存活及轴突再生的作用。     

Neuroprotective effect of Qinggan Lishui formula on retinal ganglion cell apoptosis in a microbead-induced rat chronic glaucoma model

OBJECTIVE

To investigate a possible mechanism for protective effects of a decoction of the Qinggan Lishui formula (QF) on retinal ganglion cells (RGCs) in a rat model of microbead-induced chronic intraocular hypertension (COH).

白藜芦醇对大鼠视网膜缺血再灌注损伤后视网膜组织中Caspase-3和Bcl-2表达的影响

目的：研究白藜芦醇对大鼠视网膜缺血再灌注损伤（RIRI）后视网膜组织中Caspase-3和Bcl-2表达的影响,探讨白藜芦醇对RIRI的治疗作用及其机制。方法：选取SD大鼠90只,随机分为假手术组、模型组和治疗组,每组30只,通过对前房加压建立大鼠RIRI模型,模型组和治疗组大鼠缺血再灌注1、6、12、24和48 h,治疗组大鼠用微量注射器于大鼠玻璃体腔内注射0.5 nmol·L^-1的白藜芦醇5 μL。采用倒置显微镜观察视网膜组织结构,采用免疫组织化学法和Western blotting法检测各组大鼠视网膜组织中Caspase-3和Bcl-2的阳性细胞数和蛋白表达水平。结果：模型组大鼠造模后视网膜组织水肿,可见神经节细胞空泡样变性,细胞层排列呈现疏松状,视网膜神经节细胞数目大量减少,边界模糊,神经纤维层明显变薄;治疗组大鼠视网膜组织结构、损伤程度及神经节细胞变性程度均轻于模型组。免疫组织化学检测,与模型组比较,治疗组大鼠视网膜组织中Caspase-3和Bcl-2阳性细胞数明显升高（P<0.05）。Western blotting法检测,与模型组比较,治疗组大鼠各时间点视网膜组织中Bcl-2蛋白表达水平升高,24和48 h时差异有统计学意义（P<0.05）;治疗组各时间点大鼠视网膜组织中Caspase-3蛋白表达水平均明显降低（P<0.05）。结论：白藜芦醇对RIRI大鼠的视网膜神经节细胞结构有改善作用,其作用机制可能与降低视网膜组织中Caspase-3表达水平及升高视网膜组织中Bcl-2表达水平有关。     

Therapeutic effect of bFGF on retina ischemia-reperfusion injury

Background Basic fibroblast growth factor (bFGF) plays important roles in retina degeneration, light injury, mechanical injury, especially in retina ischemia-reperfusion injury (RIRI). This study was to investigate the therapeutical effect of bFGF on RIRI and its mechanisms.Methods Experimental RIRI was induced by increasing intraocular pressure (IOP) in the eyes of 48 rats. These rats were divided into normal control, ischemia-reperfusion and bFGF-treated groups.Histological and ultrastructural changes of in the retina of different groups were observed, and the number of retinal ganglion cells (RGCs) was quantitatively analyzed under microscopy. Apoptotic cells were detected using the TdT-dUTP terminal nick-end labeling (TUNEL) method. The expression of caspase-3 was determined by streptavidin peroxidase (SP) immunohistochemistry. Atomic absorption spectrum method was used to evaluate the intracellular calcium changes.Results At the early stage of retinal ischemia-reperfusion injury, retina edema in the treated group was significantly eliminated compared with the untreated ischemic animals. RGCs in the bFGF-treated group was more than those in the untreated ischemic group during the post-reperfusion stages. In ischemic group, apoptotic cells could be found at 6th hours after reperfusion and reached the peak at 24th hours. At 72th hours no apoptotic cells could be found. The changes in caspase-3 expression had a similar manner. The intracellular calcium of rat retina began to increase at lth hour, reached the peak at 24 hours, and began to decease at 72th hours. The change of the three markers in the treatment group showed a similar pattern, but they were all relatively less obvious.Conclusion Apoptosis may play a vital role in RIRI. bFGF may has therapeutical effects on RIRI by inhibiting the increase of intracellular calciums and caspase-3 expression.     

急性高眼压大鼠视网膜睫状神经营养因子表达变化

目的探讨睫状神经营养因子（CNTF）在急性高眼压大鼠视网膜中的定位及表达变化。方法采用前房灌注法建立大鼠急性高眼压模型,在1,3,7,14,21 d分别摘取眼球,运用RT-PCR和免疫组织化学方法检测视网膜CNTF的定位及表达变化。结果对照组大鼠视网膜神经节细胞层（GCL）有少量CNTF表达,急性高眼压大鼠视网膜CNTF的表达显著增加,建立模型后第3-7天表达量达到高峰,此时除GCL外,神经纤维层（NFL）、内核层（INL）亦发现CNTF表达,后表达减少。结论急性高眼压大鼠视网膜CNTF表达增加,可能是大鼠高眼压损伤后的一种保护性反应,CNTF的增加对视网膜神经节细胞可能有保护作用。     

多聚物-1免疫高眼压大鼠视网膜中助性T细胞的变化

目的 探讨辅助性T细胞(Th细胞)在多聚物-1( Cop-1)对高眼压大鼠视网膜神经节细胞保护中可能发挥的作用.方法 Wistar大鼠分别结扎3根巩膜上静脉,建立高眼压模型96只,完全随机法分入Cop-1免疫组48只,磷酸盐缓冲液(PBS)免疫组48只,另10只正常大鼠作对照.于免疫后3、7、10、17、24、31 d...     

HSP72在视网膜的表达及其对抗细胞凋亡作用的研究

目的:检测锌离子诱导的HSP72在大鼠视网膜的表达及HSP72对视网膜缺血再灌注损伤所致细胞病理性凋亡的抑制作用。方法:生理盐水前房加压灌注制作视网膜缺血再灌注(RIR)损伤模型,以腹腔注射硫酸锌诱导HSP72表达作为实验组,以腹腔注射HSP表达抑制剂———槲皮素作为实验对照组,以不作任何处理的大鼠为正常对照组。于不同时间段对视网膜HSP72免疫组化染色,Tunel染色、计数凋亡细胞,比较各组差异。结果:实验组在注射硫酸锌后10 h即见视网膜节细胞层有HSP72阳性表达,16 h达高峰,注射后7 d仍呈弱阳性表达,HSP72主要在神经节细胞(RGC)胞浆表达;正常对照组及实验对照组均呈阴性表达。Tunel染色显示,RIR后12 h即有病理性细胞凋亡现象,24 h明显增多,实验组凋亡细胞计数少于对照组且有统计学意义(P<0.05)。结论:(1)腹腔注射锌离子可诱导大鼠视网膜HSP72表达,注射槲皮素可抑制此作用,HSP72主要在RGC胞浆表达;(2)RIR能导致视网膜病理性细胞凋亡,HSP72具有对抗凋亡的作用。     

亚低温对大鼠视网膜缺血再灌注损伤保护作用的电镜观察

目的 观察亚低温对缺血再灌注大鼠视网膜超微结构的影响,了解亚低温对视网膜缺血再灌注损伤是否有保护作用。方法 ２４只ＳＤ大鼠随机分正常组、缺血再灌注组和亚低温缺血再灌注组,每组８只。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。用透射电镜观察各组视网膜的超微结构。结果 缺血再灌注视网膜损伤主要表现在视细胞和节细胞。视网膜视细胞外节膜盘肿胀,排列紊乱,部分膜盘脱落,椭圆体内部分线粒体肿胀,节细胞的胞浆淡而空,节细胞水肿明显,多数线粒体肿胀、空泡化,滑面内质网扩张,部分粗面内质网扩张、脱粒;少数节细胞胞膜破裂、胞浆流失。亚低温缺血再灌注视网膜的视细胞外节膜盘略见疏松,椭圆体内线粒体正常;节细胞胞膜完整,包浆内可见肿胀线粒体,但肿胀较轻,其他细胞器未见明显改变。结论 亚低温可减轻缺血再灌注视网膜病变程度,对视