神经营养因子对视网膜缺血再灌注损伤的影响

视网膜缺血再灌注损伤是由于自由基、炎性细胞因子等细胞微环境的改变引起的病理过程,能造成视网膜及神经组织严重损伤。微环境包括对细胞产生影响的周围结构和成分,如附近的神经细胞、基质细胞和结合在胞外基质上的各种生长因子和细胞因子等。这些因子有的具有保护视网膜作用,如神经生长因子、睫状神经营养因子、脑源性神经营养因子、碱性成纤维细胞生长因子等;有的具有损伤作用,如血管内皮生长因子等。本文结合文献以这些因子在视网膜缺血再灌注损伤中的作用作一综述。     

大鼠坐骨神经局部缺血对其轴浆运输的影响

目的：探讨周围神经局部缺血对其轴浆运输的影响。方法：采用Ｗｉｓｔａｒ大鼠３０只，用游离实验侧有神经的方法，制成周围神经缺血模型。于双侧腓总神经干注入３０％ＨＲＰ水溶５μｌ，动物分别存活１６、１８、２０、２、２４、４８ｈ后，经升主动脉灌流杀以腰髓４－６节段和腰４－６背根节，冰冻连切片，ＢＤＨＣ法成色。结果：实验侧在腰髓４、５节前角最早出现标记细胞的时间是２４，（对照侧是１８ｈ，实验则ＨＲＰ轴浆运输速     

缺血预处置对大鼠肢体缺血再灌注损伤的影响

目的和方法在大鼠肢体缺血再灌注（ＩＲ）损伤模型上观察了缺血预处置（ｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇ，ＰＣ）的影响。结果：发现ＰＣ可以明显减轻ＩＲ引起的血压降低，血浆乳酸脱氢酶、组织蛋白酶Ｄ活性及脂质过氧化产物丙二醛含量的升高；并抑制骨骼肌组织水肿及骨骼肌细胞线粒体钙超载的发生。同时还观察到，ＰＣ对ＩＲ时肢体微血管通透性升高、中性粒细胞浸润及血浆内皮素水平增高均有抑制作用。结论：ＰＣ对大鼠ＩＲ肢体有保护作用，其保护机理之一与其对血管床的保护作用有关。     

缺血预处置对大鼠肢体血再灌注损伤的影响

目的和方法 在大鼠肢体血再灌注（ＩＲ）损伤模型上观察了缺血预处置（ｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇ，ＰＣ）的影响，结果：发现ＰＣ可以明显减轻ＩＲ引起的血压降低，血浆乳酸脱氢酶，组织蛋白酶Ｄ活性及脂质过氧化物丙二醛含量的升高，并抑制骨骼肌组织水肿及骨骼肌细胞线粒体钙超载的发生。同时还观察到，ＰＣ对ＩＲ时肢体微血管通透性升高，中性粒细胞浸润及血浆内皮素水平增高均有抑制作用，结论：ＰＣ对大鼠ＩＲ肢体有保护     

亚低温对大鼠视网膜缺血再灌注自由基损伤的保护

目的 :探讨亚低温是否对大鼠视网膜缺血再灌注自由基损伤具有保护作用。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。应用透射电镜观察正常对照组、缺血再灌注组和亚低温缺血再灌注组三组大鼠视网膜的超微结构 ;同时测定三组大鼠视网膜组织超氧化物歧化酶 (SOD)活性和丙二醛 (MDA)的含量。结果 :缺血再灌注组大鼠视网膜视细胞外节膜盘肿胀 ,排列紊乱 ;节细胞水肿明显 ,多数线粒体肿胀 ;滑面内质网扩张 ,部分粗面内质网扩张、脱粒。亚低温缺血再灌注组视网膜的视细胞外节膜盘略见疏松 ;节细胞胞浆内可见肿胀线粒体 ,但肿胀较轻。缺血再灌注组和亚低温缺血再灌注组大鼠视网膜的SOD含量分别是 5 6 2± 1 .8nu/ml和72 .3± 2 .3nu/ml;MDA含量分别是 8.0 5 4+0 .893nmol/ml和 6.0 2 3 +0 .3 98nmol/ml。结论 :亚低温可通过抑制脂质过氧化反应和自由基的过多生成 ,对视网膜缺血再灌注损伤起保护作用。     

面神经局部缺血对其超微结构的影响

目的:观察面神经局部缺血对其超微结构的影响,为临床腮腺切除术提供参考资料.方法:选用家兔,采用同体对照的方法,模拟人腮腺切除手术.实验侧于手术显微镜下,游离面神经并破坏其外血管系,切除腮腺.术后2、3、4周分别取双侧面神经透射电镜下观察.结果:实验侧早期2周轴索内微丝呈增生性改变;中期3周以轴索内微丝破坏、线粒体肿胀变性为主;晚期4周变性轴索溶解.结论:为切除腮腺,游离面神经破坏其外血管系,可导致面神经纤维轴索变性;提示临床腮腺切除时,应尽可能保护面神经外血管系,以减少面瘫的发生.     

OCT测量分析视网膜中央静脉阻塞黄斑囊样水肿时 黄斑区视网膜厚度变化研究

目的 研究频域光学相干断层扫描仪Cirrus HD-OCT对视网膜中央静脉阻塞黄斑囊样水肿（CRVO-CME）时黄斑区视网膜厚度的变化情况。方法 纳入我院2017年11月~2019年2月收治的45例（60眼）CRVO-CME患者作为研究组,另选取45例（60眼）来我院进行体检的健康志愿者作为对照组。所有患者均行HD-OCT检查,根据早期糖尿病视网膜病变治疗研究（ETDRS）视力表对黄斑区进行分区,观察两组眼黄斑区视网膜厚度情况,分析黄斑区视网膜厚度与最佳矫正视力（BCVA）的关系。结果 研究组F、IT、II、IN、IS、OT、OI、ON以及OS黄斑区9个分区的视网膜厚度均大于对照组,差异有统计学意义（P＜0.05）。IT、II、IN、IS黄斑区4个内分区厚度组间比较,差异无统计学意义（P＞0.05）;OT、OI、ON以及OS黄斑区4个外分区厚度组组间比较,差异无统计学意义（P＞0.05）。CRVO-CME患者FT以及Fmax与BCVA存在负相关性（P＜0.05）。结论 CRVO-CME患者视网膜各分区均比正常人视网膜更厚,对CRVO-CME患者进行HD-OCT测量对视网膜厚度的判断较准确,为临床诊治CRVO-CME提供了有力依据。     

面神经局部缺血对面神经核超微结构的影响

目的：为临床腮腺切除手术提供参考资料。方法：选用家兔,采用同体对照的方法,模拟人腮腺切除手术。实验侧于手术显微镜下,游离面神经并破坏其外血管系,切除腮腺。对照侧不破坏外血管系。术后2、3、4周分别取面神经核透射电镜下观察。结果：实验侧术后3周,面神经核细胞超微结构发生了明显的病理变化,而对照侧未见明显特异性变化。结论：游离面神经破坏其外血管系切除腮腺,可导致面神经核细胞超微结构发生明显的病理变化,这可能是腮腺切除术后患者发生面瘫的另一诱因。     

复脉饮对缺血大鼠视网膜形态学及血清超氧化物歧化酶活性和一氧化氮水平的影响

目的：研究复脉饮(FMD)对实验性缺血大鼠视网膜的形态结构及其血清超氧化物歧化酶(SOD)活性和一氧化氮(NO)水平的影响。方法：用高眼压法制作Wistar大鼠视网膜缺血模型。分别以FMD、复明片(FMT)和生理盐水(SAL)于建模后喂饲3周。比色法测定各组大鼠SOD活性,硝酸还原酶法测定NO水平。光镜、电镜观察各组大鼠视网膜的结构。结果：经FMD治疗后,缺血大鼠血清SOD水平升高而NO水平降低,与SAL组有显著差异;其视网膜的分层、厚度、显微和亚微结构等明显优于SAL组,也优于FMT组。结论：FMD可能参与了抗氧化,参与了视神经细胞间信号转导通路的修复以及神经递质和调质的平衡,能有效治疗大鼠视网膜缺血性损害。     

Unusual origin of the ophthalmic artery and occlusion of the central retinal artery

Summary Any variations in the origin of the ophthalmic a. are uncommon and well-explained by the comparative anatomy and human embryology. A unique case is reported of an ophthalmic a. arising from the middle meningeal a. associated with an occlusion of the central retinal a. Embryologic variations which can give such an unusual origin are discussed. Although this association may be fortuitous, we consider that an unusual origin of the ophthalmic a. could be a further factor for an occlusion of the central retinal a.

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Variation d'origine de l'artère ophtalmique et occlusion de l'artère centrale de la rétine

Résumé Les variations d'origine de l'artère ophtalmique sont rares et bien expliquées par l'étude de l'anatomie comparée et de l'embryologie humaine. Nous rapportons le cas exceptionnel d'une variation d'origine de l'artère ophtalmique à partir de l'artère méningée moyenne associée à une occlusion de l'artère centrale de la rétine. Les variations embryologiques pouvant donner naissance à cette origine inhabituelle sont discutées. Bien que cette association puisse être totalement fortuite, nous pensons qu'une variation d'origine de l'artère ophtalmique peut constituer un facteur favorisant pour une occlusion de l'artère centrale de la rétine.

     

Urocortin 2 protects against retinal degeneration following bilateral common carotid artery occlusion in the rat

Urocortin 2 (Ucn 2) is corticotropin-releasing factor (CRF) paralog that preferentially activates CRF₂ receptors. Ucns exert CRF₂-mediated cytoprotective effects against ischemia-reperfusion injury in cardiomyocytes. However, little is known regarding potential retinoprotective effects of Ucns despite the known presence of CRF family peptides and their receptors (predominantly CRF_2α) in retina. Therefore, the present study investigated the effects of post-ischemic intravitreal Ucn 2 (2 nmol) administration on ischemia-induced retinal degeneration. Two-month-old rats were subjected to permanent bilateral common carotid artery occlusion, and their retinas were processed histologically after two weeks survival to determine the density of viable cells in the ganglion cell layer and the thickness of all retinal layers. In vehicle-treated subjects, carotid occlusion reduced retina thickness by approximately 60% as compared to sham-operated animals. In contrast, intraocular Ucn 2 treatment led to a marked amelioration of the retinal layers, and the thickness of all layers was significantly increased by 40% compared to ischemic vehicle-treated subjects. Ucn 2 treatment also increased the number of cells by 55% in the ganglion cell layer as compared to those from carotid-occluded retinas of vehicle-treated subjects. These findings suggest that intraocular Ucn 2 treatment may protect against ischemia-induced retinal degeneration, results with potential therapeutic implications for ophthalmic diseases.     

ATPase activity in macula densa cells of the rabbit kidney

Na-K- and Mg-activated ATPase activities were determined in maculae densae and glomeruli dissected from both superficial and juxtamedullary nephrons of normal rabbits, using an ultramicro method including a cycling reaction. Activities were expressed as P_i generated per macula densa or per glomerulus and normalized for tissue volume. Results indicate that the mean volume of superficial and juxtamedullary macula densa samples was not statistically different, while glomeruli from deep nephrons had sample volumes that were 29% larger than those from superficial nephrons (P<0.001). Correcting for volume both superficial and juxtamedullary macula densa samples had an Na-K-ATPase activity of 0.37±0.21 fmol · h^–1 · (m³)^–1. Mg-ATPase activity in both pools was also similar [0.41±0.07 and 0.52±0.1 fmol · h^–1 · (m³)^–1]. Na-K-ATPase activity in macula densa cells is estimated to be about 1/40th the activity of surrounding cortical thick ascending limb cells. Total glomerular ATPase per unit volume was significantly higher in glomeruli from superficial than from deep nephrons [0.41±0.04 vs. 0.28±0.04 fmol · h^–1 · (m³)^–1 P<0.05]. There was no statistically significant activity of Na-K-ATPase in either superficial or deep glomeruli. These results suggest that in contrast to previous reports, the macula densa contains Na-K-ATPase, but at a low level relative to surrounding tubular cells. Further, in normal rabbits, this activity is invariant in superficial and juxtamedullary samples.     

阿魏酸钠治疗视网膜静脉栓塞疗效观察

目的探讨阿魏酸钠注射液治疗视网膜静脉栓塞的临床效果。方法100例（100只眼）视网膜静脉栓塞患者，随机分成治疗组和对照组各50例。对照组给予常规治疗，治疗组给予阿魏酸钠注射液300mg／d静脉滴注，14d为一疗程。测定治疗前后视力、视网膜中央静脉血流速度、视网膜中央动脉平均收缩期峰值血流速度。结果应用阿魏酸钠治疗后，视力明显改善，视网膜中央静脉血流速度和收缩期峰值血流速度显著提高，与对照组治疗后相比均有显著性差异，疗效优于对照组。结论阿魏酸钠治疗视网膜静脉栓塞疗效显著。     

Role of macula densa neuronal nitric oxide synthase in renal diseases

Macula densa cells have an important role in the regulation of glomerular blood flow and glomerular filtration by its regulation of afferent arteriolar vascular tone. Nitric oxide derived from neuronal nitric oxide synthase (nNOS) in macula densa can dilate afferent arterioles. Macula densa nNOS is important for renin secretion, and its expression is regulated by dietary salt, renal angiotensin II, intracellular pH, and other factors. In salt-sensitive hypertension, nNOS is suppressed, whereas in SHR or in the early phase of diabetes, nNOS is increased in macula densa along with NADPH oxidase, which limits NO bioavailability. Renal damage induced by hypertension, diabetes, and hyperlipidemia could be prevented by enhancement of nNOS in macula densa with ACEI, dipyridamole, α₁-receptor blocker, a low-salt diet, or sodium bicarbonate. Sodium bicarbonate is a safe and clinically available enhancer of nNOS in macula densa that increases glomerular blood flow and prevents the reduction of GFR in radiocontrast nephropathy and chronic renal failure. In conclusion, the enhancement of nNOS in the macula densa can be a promising strategy to prevent reduction of renal function.     

Retinal protective effects of topically administered agmatine on ischemic ocular injury caused by transient occlusion of the ophthalmic artery

Agmatine, an endogenous polyamine and putative neuromodulator, is known to have neuroprotective effects on various neurons in the central nervous system. We determined whether or not topically administered agmatine could reduce ischemic retinal injury. Transient ocular ischemia was achieved by intraluminal occlusion of the middle cerebral artery of ddY mice (30-35 g) for 2 h, which is known to also induce occlusion of the ophthalmic artery. In the agmatine group (N = 6), a 1.0 mM agmatine-containing ophthalmic solution was administered four times daily for 2 weeks before occlusion. In the control group (N = 6), a 0.1% hyaluronic acid ophthalmic solution was instilled at the same times. At 22 h after reperfusion, the eyeballs were enucleated and the retinal sections were stained by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Transient ocular ischemia induced apoptosis of retinal cells in the entire retinal layer, and topically administered agmatine can significantly reduce this ischemic retinal injury. The proportion of apoptotic cells was definitely decreased (P < 0.001; Kruskal-Wallis test). Overall, we determined that topical agmatine application effectively decreases retinal damage in an in vivo ocular ischemic injury model. This implies that agmatine is a good candidate as a direct neuroprotective agent for eyes with ocular ischemic diseases.     

Hyperbaric oxygenation mitigates focal cerebral injury and reduces striatal dopamine release in a rat model of transient middle cerebral artery occlusion

The usefulness of the administration of hyperbaric oxygen (HBO) in the treatment of acute focal cerebral ischemia remains debatable. A significant association exists between focal cerebral injury and an excessive release of extracellular dopamine (DA). In vivo microdialysis was used in the present study to examine the effect of HBO on DA release in the striatum during ischemia and reperfusion in rats. The histological changes occurring were also evaluated. Focal cerebral ischemia was induced by occlusion of the middle cerebral artery (MCA) using a surgically placed intraluminal filament. Control rats (n=8) were subjected to 1 h of ischemia, whilst the study rats (n=8) were in addition treated with HBO (2.8 atmospheres of absolute pressure 100% O₂) during ischemia. Both groups were returned to breathing room air at normal pressure during reperfusion. Microdialysis samples were continuously collected at 15 min intervals at 2 μl·min^–1. The [mean (SE)] increase in release of striatal DA attained significance after 30 min of occlusion of MCA [170 (24)%], and continued to increase [268 (26)% at 45 min] reaching a peak level at 60 min [672 (59)%] before returning to the baseline level during the late reperfusion phase. There was no significant change in the level of DA in HBO treated rats during the period of ischemia. A significant reduction in edema and neuronal shrinkage were observed by histological examination in HBO treated rats when compared to the control rats. The results showed that HBO, when administered during ischemia, offered significant neuroprotection in our experimental model of transient focal cerebral ischemia in the rat. The mechanism seems to imply, at least in part, a reduced level of DA. Electronic Publication     

SD大鼠视网膜中央动脉的应用解剖学研究

目的　为建立稳定可靠的视神经损伤动物模型寻求解剖学依据。 方法　用红色乳胶灌注技术显示正常SD大鼠视网膜中央动脉的来源、分支、分布及其与视神经的关系,并采用体视显微镜摄片测量;明胶墨汁灌注技术显示距眼球后极2.0 mm或6.0 mm处横断视神经后视网膜的血供。 结果　视网膜中央动脉及其分支在视神经鞘内始终与视神经干伴行,视网膜中央动脉起始部到眼球后极的距离为(5.784±0.054)mm;距离眼球后极6.0 mm处鞘内视神经横断组大鼠视网膜单位面积血管数目高于其他部位横断组。 结论　在制备视神经损伤SD大鼠模型时,损伤视神经应在鞘内进行,损伤部位距眼球后极　6.0 mm最佳。     

Post-treatment of a BiP inducer prevents cell death after middle cerebral artery occlusion in mice

We previously reported the effect of a selective inducer of BiP (a BiP inducer X; BIX) after permanent middle cerebral artery occlusion (MCAO) in mice. However, in acute stroke, almost all drugs have been used clinically after the onset of events. We evaluated the effect of post-treatment of BIX after permanent MCAO in mice, and examined its neuroprotective properties in in vivo mechanism. BIX (intracerebroventricular injection at 20 μg) administered either at 5 min or 3 h after occlusion reduced both infarct volume and brain swelling, but at 6 h after occlusion there was no reduction. BIX protected against the decrease in a dose-dependent manner. Furthermore, BIX reduced the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells induced by the ischemia in ischemic penumbra. These findings indicate that post-treatment with BIX after ischemia has neuroprotective effects against acute ischemic neuronal damage in mice even when given up to 3 h after MCAO. BIX may therefore be a potential drug for stroke.