白内障摘出术后眼压增高的治疗

本文研究匹罗卡品凝胶剂、匹罗卡品溶液和噻吗心安对白内障囊外摘出术后眼压增高的作用。80例拟行常规白内障囊外摘出术联合后房型人工晶体植入术的患者随机分为4组,每组20眼。Ⅰ组点4％匹罗卡品凝胶剂,Ⅱ组点4％匹罗卡品溶液,Ⅲ组点0.5％噻吗心安溶液,Ⅳ组点0.5％平衡盐溶液(安慰剂)。于手术前一天上午8时及下午2时用Goldmann压平眼压计测量     

用噻吗心安和肾上腺素治疗开角型青光眼

本文对联合应用噻吗心安和肾上腺素与联合应用噻吗心安和匹罗卡品治疗原发性开角型青光眼的疗效进行比较。并对有关噻吗心安和肾上腺素的文献进行研究。 32例患者64眼先用0.25%噻吗心安每日2次共用2周,3人未能坚持,其余29例中14例加用0.1％肾上腺素每日2次,15例加用2％匹罗卡品每日4次,持续3个月以上,检查视力、眼压、外眼及裂隙灯检查,视乳头及视野检查,研究结果表明:噻吗心安和匹罗卡品合用比噻吗心安和肾上腺素合用临床降低眼压方面更有效.尽管差别无统计学意义。用噻吗心安和epinephrine(为一拟肾上腺     

预先应用噻吗心安对Nd：YAG激光后囊切开术后的眼压观察

本文应用 Nd:YAG 激光后囊切开术的64只眼,术前随机对其中的32只眼给予5mg/ml(0.5%)噻吗心安滴眼,另外32只眼不用任何药物作为对照.结果表明,激光治疗后4小时内,术前用药组的平均眼压升高显著地低于对照组(P<0.01),并于术后第2小时降压效果最明显.此外,术后24小时和48小时用药组的眼压升高仍低于对照组,但两者的差别无显著性(P>0.05).作者认为 Nd:YAG 激光后囊切开术前预先用噻吗心安滴眼,可减轻术后的急性眼压升高。虽不能完全预防后期的眼压升高,亦可减轻其眼压升高的程度。因此,噻吗心安可作为 Nd:YAG 激光后囊切开术前的常规用药,以减轻术后高眼压的不良反应.     

顽固性闭角型青光眼的治疗

作者介绍一种治疗顽固性急性闭角型青光眼的方法,并用这种方法治疗17例(17眼)局部曾用过噻吗心安、匹罗卡品和口服乙酰唑胺无效的急性闭角型青光眼患者,取得了成功。方法如下:患者被确诊为急性闭角型青光眼后,若无明显恶心,即给予乙酰唑胺500mg口服。患眼点0.5％噻吗心安一滴,接着点4％匹罗卡品眼药水,每隔10分钟点3滴。如果30分钟后眼压不下降,则球后注射2％利多卡因     

噻吗心安的急性过敏反应

噻吗心安是一种β-肾上腺素能受体阻滞剂,业已广泛用于治疗青光眼。该药有心动过缓的副作用,但尚无急性过敏反应的报导,作者报告一例女性,67岁。患闭角型青光眼近5年,周边虹膜切除术后加用2%匹罗卡品眼压控制。因有核性白内障,为改善视力给滴用0.25%的噻吗心安。在滴后2小时,双眼剧痛,视力模糊及大量分泌物,双眼睑水肿,结膜充血及小出血点,角膜和前房无异常。实验室检查无特殊发现。作者当时认为是腺病毒感染。经用药反应消退后仍用匹罗卡品治疗。3个月后再次对病人使用噻吗心     

用噻吗心安及缩瞳剂治疗急性闭角型青光眼

噻吗心安系抑制房水生成的β-肾上腺素能受体阻滞剂,可有效的治疗原发性开角型青光眼(Zimmerman等1977)、继发性青光眼(Saai 1978),但治疗晶体囊性青光眼无效(Kerty等1978)。尚未见有对闭角型青光眼有降压效果的报告。在闭角型青光眼单用噻吗心安不能有效的控制眼压,但在滴噻吗心安后继用匹罗卡品则会有好的降压效果。     

噻吗心安、匹罗卡品混合滴用和单独滴用的对比

噻吗心安眼液于1978年首先在瑞典用于眼科临床,现已成为最常用的降眼压药物。它是β-肾上腺素能阻滞剂,通过减少房水生成而降低眼压。临床上,有些青光眼病人尚需配用其它药物,匹罗卡品属首选。匹罗卡品是胆硷能药物,其主要作用是使前房水易于外流。     

氟哌啶降眼压作用研究(第一部分:氟哌啶对猕猴及家兔的降眼压作用)

青光眼是致盲的主要眼疾之一,对青光眼进行有效的药物治疗是防盲治盲的重要措施。目前临床常用于治疗青光眼的药物主要有匹罗卡品、噻吗心安和醋氮酰胺,但这些药物的降服压效果不甚理想,且常引起一些副作用。匹罗卡品是一种拟胆硷能药物,可引起明显缩瞳、睫状肌痉挛、头痛、视力模糊等副作用;噻吗心安是肾上腺β受体阻断剂,可引起心动     

抗青光眼药物的最新进展

用于治疗开角型青光眼的药物,依其作用的基本方式,可分为三种主要类型:(1)使房水排出增加,而不影响房水生成的药物。例如胆碱能兴奋剂(匹罗卡品和N-脱甲基氨甲酰胆碱);胆碱酯酶抑制剂(毒扁豆碱和二乙氧膦酰硫胆碱);以及房水排出阻力减低剂(依地酸和细胞松弛素B)。(2)使房水生成减少,而不影响房水排出的药物。如碳酸酐酶抑制剂(乙酰唑胺)和β-肾上腺素能阻断剂(噻吗心安)。(3)对房水排出和生成都有影响的药物。如肾上腺素能兴奋剂(肾上腺素和异丙肾上腺素),以及大麻。青光眼的治疗,从匹罗卡品和毒扁豆碱应用于临床一百多年以来,几无甚进展。直到1977年发现了噻吗心安,才有所突破。一、噻吗心安(Timolol) 该药是一种β-肾上腺素能阻断剂(以下简称β阻断剂)。1978年该药以商品名称“Timoptic”首次投放市场。噻吗心安对正常人和青光眼患者都有降低眼压的作用,且作用迅速。临床使用噻吗心安的浓     

拉坦前列素治疗残余性闭角型青光眼的临床研究

目的观察拉坦前列素用于外滤过或虹膜周切术后的残余性闭角型青光眼的降眼压效果。方法采用随机、单盲、平行对照试验,选取外滤过或虹膜周切术后的残余性闭角型青光眼患者(眼压≥21mmHg且≤35mmHg,前房角检查至少累计90度范围内看到部分睫状体带),拉坦前列素组每晚一次,噻吗心安对照组早、晚各用一次,共观察8周。分别记录用药前、用药后1周、2周、4周、8周9am以及用药前、用药后8周4pm的眼压值。结果拉坦前列素组入选25例(25只眼),噻吗心安组入选24例(24只眼),两组用药后眼压都明显下降,拉坦前列素组从用药前的(24.73±3.90)mmHg(1mmHg=0.133kPa)降至8周时的(16.08±3.86)mmHg,下降幅度为35.0%;噻吗心安组从(26.00±4.44)mmHg降至(17.53±3.97)mmHg,下降幅度为32.6%。不同时间点上午两组眼压没有显著差异,而用药后8周4pm拉坦前列素组的眼压(15.33±3.16)mmHg明显低于噻吗心安组(18.76±4.13)mmHg(t=-3.016,P<0.05)。结论拉坦前列素可有效降低外滤过或虹膜周切术后的残余性闭角型青光眼的眼压,其作用较噻吗心安更持久。     

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.