准分子激光屈光性角膜切削术后角膜的组织形态改变

目的 动态观察准分子激光屈光性角膜切削术（ＰＲＫ）后角膜修复过程中的组织形态改变。方法 ２４只兔右眼按近视－１０．００Ｄ行ＰＲＫ术。按术后即刻、２４小时、１、２周、１、３、６月及１２月８个时间点观察,每个时间点３只。裂隙灯显微镜检查各组角膜上皮修复及角膜雾状浑浊（ｈａｚｅ）情况,并取角膜行光镜及电镜观察。结果 ＰＲＫ术后早期角膜上皮易剥脱,ｈａｚｅ的发生率为１００％。ＰＲＫ术后角膜上皮增生;新合成     

准分子激光兔角膜切削术后细胞凋亡和增殖

目的 寻找准分子激光角膜切削术（ＰＲＫ）术后细胞凋亡和激活增殖的动态联系,评价激光去除上皮（ＰＴＫ）和机械刮除上皮（ＭＥＳ）对凋亡和增殖的影响。方法 对１８只兔按ＰＴＫ和ＭＥＳ行ＰＲＫ（－９．９０Ｄ,６．０ｍｍ直径）,术后定期用活体共聚焦显微镜观察及制作病理切片,ＴｄＴ介导ｄＵＴＰ缺口末端标记（ＴＵＮＥＬ）原位显示凋亡细胞,激光扫描共聚焦显微镜观察凋亡细胞形态,定量统计比较凋亡水平差别。结果 ＰＲ     

准分子激光角膜切削术后屈光回退伴角膜雾浊再次手术疗效

近视眼准分子激光角膜切削术（ｐｈｏｔｏｒｅ－ｆｒａｃｔｌｖｅｋｅｒａｔｅｃｔｏｍｙ，ＰＲＫ）后，部分病例存在远期屈光回退、角膜雾浊（Ｈａｚｅ）影响疗效。我院ＰＲＫ中心于１９９６年８月～１９９７年２月对６例８眼ＰＲＫ术后屈光回退伴角膜Ｈａｚｅ病例行再次ＰＲＫ治疗，效果满意，总结报道如下。１材料与方法１．１临床资料８眼病例为我院ＰＲＫ中心治疗后随访１１．２±１．４ｍｏ出现屈光回退伴角膜Ｈａｚｅ的近视眼患者，男６眼，女２眼，年龄２４．０±４．０６ａ（１９～４０ａ）。首次ＰＲＫ术前平均等值球镜屈光度为一…     

准分子激光对角膜内皮细胞影响的实验研究

目的 观察激光角膜光学切除术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅ ｋｅｒａｔｅｃｔｏｍｙ,ＰＲＫ）对角膜内皮细胞损伤的可能性。方法 采用有血清和无血清培养正常兔角膜和ＰＲＫ切削深１５０μｍ角膜１ｗｋ后,观察内皮细胞形态和内皮细胞密度。结果 ＰＲＫ切削深１５０μｍ无血清培养１ｗｋ后,角膜内皮细胞形态、大小不一,部分细胞边界染色较宽,内皮细胞密度明显低于对照组（Ｐ〈０．０５）。ＰＲＫ切削深１５０μｍ有血清     

准分子激光屈光性角膜切削术后角膜上皮愈合的临床研究

准分子激光屈光性角膜切削术后角膜上皮愈合的临床研究昆明部队总医院眼科雷鸣，宫枢政，张仲彦，李旭松，姚建玲准一分子显光屈光性角膜切削术｛６ｈｏｌｏｕｄｄ仍ｗＫｅｒａｔｅｃｔｏｍｙ，ＰＲＫ）是近年来发展起来改一种新的治疗屈光不正的手术方一法ｌ‘。”．、手...     

羊膜对激光角膜切除术后TGF—β1表达调控的初步研究

目的 探讨羊膜对激光角膜光学切除术（Ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅ ｋｅｒａｔｅｃｔｏｍｙ ＰＲＫ）后角膜组织ＴＧＦ－β１表达的影响。方法 对６只新西兰白兔双眼行ＰＲＫ,术后１眼立即行角膜表面羊膜移植术,只眼作为对照。术后４周用原位杂交方法检测角膜上皮和基质ＴＧＦ－β１ｍＲＮＡ的表达。结果 ＰＲＫ后４周对照组角膜上皮和基质有较浓度的ＴＧＦ－β１ｍＲＮＡ表达,羊膜移植组角膜上皮和基质亦有ＴＧＦ－β１     

准分子激光屈光性角膜手术后角膜知觉的改变

目的观察和分析准分子激光屈光性角膜切削术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ，ＰＲＫ）和准分子激光原位角膜磨镶术（ｌａｓｅｒｉｎ－ｓｉｔｕｋｅｒａｔｏｍｉｌｅｕｓｉｓ，ＬＡＳＩＫ）治疗近视后角膜知觉的变化。方法对２３１例（３８７只眼）近视患者施行ＰＲＫ，对４８２例（７９６只眼）施行ＬＡＳＩＫ进行治疗。对术后角膜知觉不同时期的变化进行检查、分析。结果ＰＲＫ和ＬＡＳＩＫ术后早期角膜知觉均明显下降，尤以ＰＲＫ明显。ＰＲＫ术后角膜知觉在术后６个月才能恢复，ＬＡＳＩＫ术后角膜知觉约在术后１个月即恢复。结论ＰＲＫ术后角膜知觉的恢复比ＬＡＳＩＫ慢。     

家兔角膜准分子激光切削术后病理学观察

目的对近期准分子激光角膜切削术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ，ＰＲＫ）后角膜伤口变化进行组织病理学观察。方法应用１９３μｍ扫描式准分子激光对８只实验兔眼行光学角膜切削术并于术后２月时组织病理学检查。结果切削区角膜表面光滑，均匀一致，上皮轻度增厚；基底膜再生，但呈厚薄不一、不连续等不成熟表现，上皮和实质层仍存在散在裂隙；基质处大部分新生胶原纤维排列有序，但局部浅实质层可见角膜细胞增多等瘢痕样改变。结论兔眼ＰＲＫ术后２月显示，组织结构基本正常，但仍存有组织薄弱处和特殊性改变。强调半桥粒－基底膜复合体在ＰＲＫ上皮修复中的意义。     

放射状角膜切开术后残余近视眼的准分子激光角膜切削术

目的探讨准分子激光角膜切削术（ＰＲＫ）矫治放射状角膜切开术（ＲＫ）后残余近视眼的安全性与有效性。方法应用ＣＨＩＲＯＮ公司ＴｅｃｈｏｌａｓＫｅｒａｃｏｒｌ１６型准分子激光机对１６例（２１只眼）ＲＫ后残余近视眼施ＰＲＫ，应用计算机辅助的角膜地形图对手术的有效性与安全性作客观评估。结果１６例（２１只眼）经ＰＲＫ后，裸眼视力提高４～１０行（平均７．５行）；等效球镜的屈光度下降２．５０～６．００Ｄ（平均４．７５Ｄ）；所有术眼的角膜地形图提示角膜中央呈规则圆形变扁区，角膜中央３ｍｍ直径的屈光力平均下降４．２５Ｄ。随访期内（１ａ）所有术眼无明显并发症。结论ＰＲＫ是矫治ＲＫ后残余近视眼安全有效的方法     

准分子激光屈光性角膜切削术后角膜地形图分析

目的分析准分子激光屈光性角膜切削术（ｐｈｏｔｏｒｅｆｒａｃｔｉｖｅｋｅｒａｔｅｃｔｏｍｙ,ＰＲＫ）术后角膜切削区的形态、偏心情况和屈光的稳定性。方法对３１２例（３６６只眼）ＰＲＫ手术患者进行术后１、３和６个月的角膜地形图检查。结果术后１个月切削区中心偏离瞳孔中心的距离为０．２６６ｍｍ,双眼平均偏离瞳孔中心的方向均为鼻上侧。切削区形态平滑型占４９．５％,半环型、钥匙洞型、肾型和哑铃型占４２．９％,中心岛型占６．０％。中心岛型对术后最佳矫正视力影响较大。术后１～３个月角膜屈折力变化较大,高度近视比低度近视回退明显。结论提示ＰＲＫ术中瞄准中心问题非常重要,直接影响术后的效果,同时也应长期随访角膜地形图,进一步观察术后的稳定性。     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.