遮盖法与阿托品散瞳法治疗弱视的疗效比较

目的：探讨遮盖法与阿托品散瞳法治疗弱视的疗效;方法：对进行弱视治疗的患分成两个组,遮盖组完成或间断遮盖优势眼,阿托品组每月或隔日滴1％阿托品水于优势眼,4周复查视力,注视性质,立体视觉。结果：遮盖法与阿托品散瞳法治疗弱视疗效无差异。结论：两种方法治疗弱视有显疗效。     

Proparacaine-Induced Mydriasis During Strabismus Surgery

Aim: To evaluate the mydriatic effect of proparacaine hydrochloride (PH) in children undergoing strabismus surgery under general anesthesia (GA). Methods: This was a pilot, prospective, non-randomized, self-controlled interventional study. Nine children with esotropia or exotropia undergoing horizontal muscle squint surgery under GA at a tertiary eye care center were included. The six Group 1 patients underwent both eye surgeries, while the three Group 2 patients underwent single eye surgery. PH was instilled in one eye of Group 1 patients and both eyes of Group 2 patients. Change in pupil diameter (PD) was analyzed as the main outcome measure. Results: Mean age of the patients was 4.67 ± 2.64 years. In the study eyes, mean average baseline PD was 1.59 ± 0.40 mm (range: 1.06–2.37), while postoperative average PD was 3.99 ± 1.34 mm (range: 1.79–6.02). The mean baseline PC had increased from 5.51 ± 1.09 mm to 12.6 ± 3.58 mm at the end of the surgery. PD and PC increased in all of the study eyes while no change in PD or PC was seen in the control eyes of either of the groups. The dilated pupil was skewed horizontally towards the muscle being operated upon in all of the study eyes. Conclusions: PH has a mydriatic effect of its own. It penetrates through the bare sclera and leads on to skewed dilation of the pupil. Surgeons should consider this effect while judging pupil alignment at the end of the surgery.     

Measurements of cycloplegia and mydriasis induced by three common ophthalmic drugs

The time course of the effects of three drugs on accommodation was assessed using conventional subjective methods and by an objective infra-red optometer, over a time period of up to three hours after drug instillation. Pupil diameter was monitored using the television display of the optometer. 1% and 0.5% Cyclopentolate, 0.5% Tropicamide and 10% Phenylephrine were separately employed on the same five subjects. The cholinergic antagonists Cyclopentolate and Tropicamide had similar initial time courses for both cycloplegic and mydriatic effects. Tropicamide typically produced incomplete cycloplegia with a short duration, and recovery was essentially complete after three hours. Cyclopentolate left only a small amount of residual accommodation of variable duration: the effects of the 1% and 0.5% concentrations employed were very similar. Subjective and objective assessments of amplitude of accommodation showed similar time courses. The adrenergic drug 10% Phenylephrine produced only a small cycloplegic effect of variable time course. Mydriatic effects of the cholinergic drugs showed similar initial time courses to the cycloplegic effects: no recovery occurred before the experimental session was complete. 10% Phenylephrine produced less mydriasis than the cholinergic drugs: the duration of the mydriasis was variable and recovery began within the experimental session. Intersubject variability occurred for both mydriatic and cycloplegic effects.     

Improving the ocular absorption of phenylephrine

An oxazolidine prodrug of phenylephrine and the base form of phenylephrine were synthesized, suspended in sesame oil, and tested for mydriatic activity against phenylephrine HCl. The HCl salt was formulated as a viscous aqueous solution and as a sesame oil suspension. A dosing volume of 10 microliter was instilled into rabbit eyes and the pupillary diameter was measured over time. A 0.045 M prodrug suspension was judged equal in mydriatic activity to a 0.45 M viscous solution of phenylephrine HCl with the exception that the time of maximum response occurred 60 min earlier with the prodrug. When phenylephrine base was suspended in sesame oil at 0.045, 0.12, and 0.45 M, the mydriatic activity was also greater than equimolar suspensions of phenylephrine HCl. The pH of tear fluids was also measured over time and found to rise 1.1, 0.70, and 0.30 pH units for 0.45, 0.12, and 0.045 M suspensions of the base form but remain unchanged when phenylephrine HCl was instilled in the rabbit eye. The greater activity associated with the base form of phenylephrine was judged a result of the change in pH to favour the absorption of phenylephrine. This latter approach should be applicable to either weak acids or weak bases with pKa values outside of the normal pH range (7-8) of the tears and in concentrations greater than 0.045 M suspended in a non-aqueous vehicle.     

Tolerance to the mydriatic effect of buprenorphine,butorphanol, nalbuphine,and cyclorphan,and cross-tolerance to morphine in mice

An increase in the use of opioid derivatives in the treatment of pain syndrome in clinical practice, and especially in the treatment of cancer, has added impetus to the search for an agent which does not induce tolerance and cross-tolerance to other opiodis. The mydriatic effect of opioids in mice, the correlation between analgesia and mydriasis, and tolerance to the analgesic effect of morphine in mice were evaluated previously. In the present work, tolerance to the mydriatic effect of four agonist-antagonists and cross-tolerance to morphine were examined. Measurement of the pupillary diameter was performed using a binocular operating microscope. Tolerance and cross-tolerance to morphine were developed following a chronic use of buprenorphine, nalbuphine, and cyclorphan. After chronic injection of butorphanol, no tolerance or cross-tolerance to morphine was observed.     

The relative potencies of cholinomimetics and muscarinic antagonists on the rat iris in vivo: effects of pH on potency of pirenzepine and telenzepine

Summary The effects of cholinomimetics and muscarinic antagonists were compared following topical administration to the eyes of anaesthetized rats. For tests with cholinomimetics, clonidine (0.3 mg/kg) was used to induce mydriasis via central inhibition of parasympathetic tone. Full, dose-dependent miosis was induced by acetylcholinesterase inhibitors [physostigmine > neostigmine > tetrahydroaminoacridine (THA)] and by membrane channel blockers (4-aminopyridine > 3,4-diaminopyridine). Oxotremorine was the most potent direct agonist tested [oxotremorine > arecaidine propargylester (APE) > arecolne > carbachol > ethoxyethyltrimethyl-ammonium iodide (EOE) > RS 86]. Some putative M1 selective agonists were weakly active or behaved as partial agonists (pilocarpine > AH6405 > Mc-A-343 > isoarecoline). Of the antagonists, compared in non-clonidine treated rats, scopolamine hydrochloride was the most potent. Of the receptor selective antagonists the M₂ (ileal) selective compounds hexahydrosiladifenidol and 4-DAMP were more potent than either M₁ selective (pirenzepine, telenzepine) or M₂ (atrial) selective (AF DX 116) drugs. These data tentatively suggest the involvement of an M₂ (ileal) type muscarinic receptor. Potency was lower for quaternary structures, probably due to impaired corneal penetration. The potency of pirenzepine and telenzepine was increased 60-fold at low pH following topical administration. Acid induced corneal damage does not appear to account for this potency shift as the effects of scopolamine and several agonists (oxotremorine, pilocarpine and McN-A-343) were not substantially altered by acid media. For pirenzepine the potency shift appears to be related to protonation of the second amino group (N1) in the piperazine tail (pK _a = 2.05). Intraocular injections suggest that diprotonation facilitates penetration through the cornea. This anomalous behaviour of pirenzepine may contribute to its potency in gastric acid inhibition where the acid environment of the stomach would favour the diprotonated state and therefore penetration through the epithelium. Send offprint requests to J. J. Hagan at the above address     

Why patients with Alzheimer’s disease may show increased sensitivity to tropicamide eye drops: role of locus coeruleus

Rationale Patients suffering from Alzheimer’s disease (AD) may show increased sensitivity to tropicamide, a muscarinic cholinoceptor antagonist. AD is associated with a severe loss of noradrenergic neurones in the locus coeruleus (LC), which can be “switched off” experimentally by the α₂-adrenoceptor agonist clonidine. The possibility arises that increased pupillary sensitivity to tropicamide in AD may be due to diminished LC activity. Objective To examine the hypothesis that clonidine may potentiate tropicamide-evoked mydriasis. Materials and methods Sixteen healthy male volunteers participated in two experimental sessions (0.2 mg clonidine or placebo) conducted 1 week apart. In each session tropicamide (0.01% 10 μl×2) was applied to the left eye and artificial tear (10 μl×2) was applied to the right eye. Pupillary functions (resting pupil diameter and light and darkness reflexes), alertness and non-pupillary autonomic functions (blood pressure, heart rate, core temperature and salivary output) were measured. Data were analysed by ANOVA, with multiple comparisons. Results Tropicamide increased resting pupil diameter, velocity and amplitude of the darkness reflex response, and decreased recovery time of the light reflex response. Clonidine affected all these pupillary measures in the opposite direction with the exception of the recovery time. The mydriatic response to tropicamide was potentiated by pre-treatment with clonidine. Clonidine reduced critical flicker fusion frequency, subjective alertness, blood pressure, salivation and temperature. Conclusions The potentiation of tropicamide-evoked pupil dilatation by clonidine may be due to the abolition of the increase in parasympathetically mediated pupil constriction due to reduced LC activity.     

依据调节功能评估10～15岁儿童近视显然验光准确性

目的观察分析10～15岁调节功能正常、超前、滞后的近视儿童显然验光与1%阿托品眼用凝胶散瞳验光结果的一致性,以指导儿童近视的验光配镜工作。方法前瞻性研究。等距随机抽样2013年7-8月间来唐山市眼科医院视光学诊疗中心就诊的近视患者224例（448眼）,按调节功能分为正常（107眼）、超前（152眼）及滞后（189眼） 3组,各自对比散瞳前显然验光、散瞳验光及瞳孔恢复后复查验光屈光度的变化。采用方差分析进行数据检验。结果调节功能正常组和滞后组3次验光所测得结果差异无统计学意义（F=0.87、0.76,P>0.05）;调节超前组3次验光所得结果差异有统计学意义（F=1.31,P<0.05）。结论10～15岁近视儿童验光配镜时,调节功能滞后和正常患者综合验光仪显然验光结果可直接用于指导配镜,对于调节超前的患者,需要以阿托品散瞳验光结果为依据。