Comparison of the effects of chronic administration of ciclazindol and desipramine on pupillary responses to tyramine, methoxamine and pilocarpine in healthy volunteers.

Twenty-nine healthy volunteers participated in an experiment lasting for 8 weeks: Phase I (2 weeks)--pre-treatment control period; Phase II (4 weeks)--medication with either ciclazindol hydrochloride (50 mg twice daily), or desipramine hydrochloride (50 mg twice daily) or lactose placebo (twice daily) administered in a single-blind fashion; Phase II (2 weeks)--recovery. Experimental sessions took place twice weekly for the photographic assessment of resting pupil diameter, and for the assessment of one of the following pupillary responses: mydriatic response to methoxamine, mydriatic response to tyramine, miotic response to pilocarpine. Resting pupil diameter increased during medication with either ciclazindol or desipramine. Methoxamine-evoked mydriasis and tyramine-evoked mydriasis were antagonized by both ciclazindol and desipramine. Pilocarpine-evoked miosis was potentiated by both ciclazindol and desipramine. The steady-state plasma levels (mean +/- s.e. mean) of the antidepressants were: ciclazindol: 5.90 +/- 0.74 microM; desipramine: 0.60 +/- 0.17 microM. The antagonism of methoxamine-evoked mydriasis is likely to reflect the blockade of postsynaptic alpha 1-adrenoceptors in the iris by the antidepressants, whereas the antagonism of tyramine-evoked mydriasis may reflect both the blockade of uptake of tyramine into presynaptic adrenergic terminals and the blockade of postsynaptic alpha-adrenoceptors. There is no immediate explanation for the potentiation of pilocarpine-evoked miosis by the two antidepressants.     

Comparison of the effects of clonidine on tyramine- and methoxamine-evoked mydriasis in man

1 It has been reported previously that clonidine can potentiate tyramine-evoked mydriasis on the pain-free side of cluster headache patients. We examined whether a single oral dose of clonidine (200 μg) can also potentiate tyramine-evoked mydriasis in healthy subjects, using mydriasis to methoxamine, a directly acting sympathomimetic amine, as a control. 2 Eight healthy male volunteers participated in four weekly sessions. In the first two sessions (Experiment 1) the effect of clonidine or placebo on the mydriasis to tyramine hydrochloride eyedrops (75 mm; 2×10 μl), and in the last two sessions (Experiment 2) the effect of clonidine or placebo on the mydriasis to methoxamine hydrochloride eyedrops (20 mm; 2×10 μl) was examined. In both experiments subjects were allocated to drugs and sessions according to a double-blind balanced design. In both experiments, pupil diameter of both the treated and the untreated eyes was recorded in standard ambient light and in the dark, before, and 2 h after clonidine/placebo, via binocular infrared television pupillometry. Salivation (dental roll technique), systolic and diastolic blood pressure (sitting), heart rate, and self-ratings of mood and feelings (visual analogue scales), were also measured before, and 2 h after the ingestion of clonidine or placebo. 3 Both tyramine and methoxamine produced a significant mydriasis, which was more prominent in the light condition (change in resting pupil size; mm±s.e.mean: tyramine/light 1.05±0.28; tyramine/dark: 0.73±0.15; methoxamine/light: 1.65±0.28; methoxamine/dark: 0.85±0.15). Clonidine produced a significant miosis in the untreated eye which was more prominent in the light condition (change in resting pupil size; mm±s.e.mean: Experiment 1, light: −1.34±0.19; Experiment 1, dark: −0.46±0.1; Experiment 2, light −0.97±0.18; Experiment 2, dark: −0.29±0.17). Clonidine had no significant effect on either tyramine- or methoxamine-evoked mydriasis. 4 In agreement with previous reports, clonidine significantly reduced salivation (g, mean±s.e.mean; Experiment 1: −0.84±0.22; Experiment 2: −0.55±0.11), systolic blood pressure (mm Hg; Experiment 1: −17.5±3.76; Experiment 2: −23.38±4.67), diastolic blood pressure (mm Hg; Experiment 2: −12.38±2.05), alertness (mm; Experiment 2: −24.19±5.40), and anxiety (mm; Experiment 1: −13.82±4.60), indicating the presence of pharmacodynamically effective tissue levels of the drug. 5 These results show that a single oral dose (200 μg) of clonidine causes significant miosis in human subjects, and fails to potentiate tyramine-evoked mydriasis. This indicates that the pupil on the asymptomatic side of cluster headache patients is affected differently from the pupils of healthy volunteers by tyramine and/or clonidine.     

Consensual pupillary responses to mydriatic and miotic drugs.

1. Three experiments were conducted to examine whether mydriatic or miotic drugs instilled into one eye have any effect on the diameter of the pupil of the untreated fellow eye, in healthy volunteers. 2. In Experiment 1, the effects of four subjects, using photography in an illuminated room to assess pupil diameter. The drug evoked a dose-dependent mydriasis in the index eye which was accompanied by a simultaneous dose-dependent miosis in the fellow eye. 3. In Experiment 2, the same method was used to assess pupil diameter as in Experiment 1. The effects of mydriatic (methoxamine and tyramine) and of miotic (pilocarpine) drugs instilled into the fellow eye, were studied on the sizes of pupillary responses to the same drugs instilled into the index eye. The presence of a mydriatic drug in the fellow eye resulted in a decrease in the size of the mydriatic responses in the index eye. 4. In Experiment 3, the effects of three concentrations of phenylephrine hydrochloride (0.15-0.60 M) and of three concentrations of pilocarpine hydrochloride (0.002-0.008 M), were studied in darkness using an infra-red binocular television pupillometer, in seven subjects. Phenylephrine evoked dose-dependent mydriasis and pilocarpine evoked dose-dependent miosis. The pupillary responses of the index eye were not accompanied by any changes in the diameter of the pupil of the fellow eye. 5. It is concluded that drug-induced mydriasis in the index eye is accompanied by a consensual miosis in the fellow eye.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ocular Pharmacokinetics and Pharmacodynamics of Phenylephrine and Phenylephrine Oxazolidine in Rabbit Eyes

The aqueous humor concentration of phenylephrine and its corresponding mydriatic response were measured over time in New Zealand albino rabbit eyes following a 10-µl topical instillation of a phenylephrine HC1 viscous solution (10%) or a phenylephrine oxazolidine (prodrug) suspension in sesame oil (1 and 10%). The bioavailability of a 1% prodrug suspension in the rabbit eye (AUC of aqueous humor concentration vs time) was 30% lower than that of a 10% phenylephrine solution (P < 0.1) with the exception that the peak time occurred 34 min earlier with the prodrug. A 10% prodrug suspension increased the aqueous humor bioavailability approximately eightfold but improved the mydriatic activity (AUC of mydriasis vs time) only fourfold. The pharmacokinetic parameters, apparent absorption, and elimination rate constants, of phenylephrine and the prodrug were determined from aqueous humor concentration–time and mydriasis–time profiles. The study showed that the kinetic parameters of phenylephrine estimated from its mydriasis profile do not accurately reflect the kinetics of drug distribution in the iris. These parameters also varied with the instillation of phenylephrine solution or prodrug suspensions. A mydriatic tolerance of the pupil response was apparent after the topical instillation of phenylephrine solution. The mydriatic tolerance may be due to the decrease in receptor number in the iris dilator muscle.     

Evaluation of the effect of thymoxamine solution 0.5% on mydriasis induced by ibopamine solution 1%

Summary The effects of thymoxamine 0.5% solution and of a placebo solution (mannitol) on the mydriasis induced by ibopamine 1% solution were evaluated in 8 healthy volunteers and 12 patients with eye diseases.One drop of ibopamine was instilled into each eye and 30 min later 1 drop of thymoxamine was instilled into one eye and 1 drop of placebo into the contralateral eye. Pupillary diameter was measured before and 30 min after the instillation of ibopamine, immediately before the treatment with thymoxamine and placebo and 30, 60 and 90 min after the instillation of thymoxamine or of placebo.Within 30 min of treatment, ibopamine had produced a statistically and clinically significant mydriatic effect. In eyes treated with thymoxamine, prompt reversal of mydriasis was observed, the baseline diameter being observed within 60 min.No difference in the time-course of the mydriatic effect was detected between healthy subjects and patients. The pupillary response to thymoxamine was not influenced by the colour of the iris. The tolerability of ibopamine and of thymoxamine was good. No local or systemic adverse events were seen or reported.     

Studies on the mechanism of clonidine-induced mydriasis in the rat

Intravenous administration of clonidine hydrochloride (3-100 micrograms/kg) produced a dose-dependent pupillary dilation in anaesthetized rats. All experiments were carried out in rats in which vagosympathetic nerve trunks were sectioned bilaterally at the cervical level. Clonidine-induced mydriasis was present only in those preparations having intact parasympathetic neural tone to the iris. Depletion of CNS monoamines by more than 95% with reserpine (5 mg/kg) and alpha-methyl-para-tyrosine (2 X 300 mg/kg) failed to alter the dose-response relation to clonidine. Pretreatment with the alpha-2-adrenoceptor antagonist, yohimbine hydrochloride (1.5 mg/kg), produced about a 10-fold shift to the right in the pupillary dose-response curve to clonidine. Yohimbine administered after the highest dose of clonidine also antagonized the mydriatic response. The above results suggest that clonidine acts on CNS post-synaptic alpha-2-adrenoceptors to produce mydriasis by withdrawal of parasympathetic neural tone to the iris. In an attempt to assess the physiological substrate(s) involved, mydriatic responses, due to parasympatho-inhibition, were evoked by electrical stimulation of ascending (sciatic nerve and medullary) and descending (hypothalamic) pathways. Yohimbine (0.3 and 1.0 mg/kg) produced a dose-dependent inhibition of the pupillary dilation evoked by stimulation of the sciatic nerve and medullary loci, whereas these doses of yohimbine failed to alter the dilation in response to hypothalamic stimulation. Similarly, monoamine depletion greatly antagonized the pupillary dilation elicited by sciatic nerve and medullary stimulation without significantly affecting mydriasis due to hypothalamic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chronic cocaine reduces alpha 2-adrenoceptor elicited mydriasis and inhibition of locus coeruleus neurons

The effects of chronic cocaine (50 mg/kg per day for two weeks) administration on two alpha 2-adrenoceptor-mediated responses were studied in rats. Chronic administration of cocaine significantly (compared to sham controls) attenuated the alpha 2-adrenoceptor-mediated inhibition of noradrenergic locus coeruleus (LC) neurons as well as alpha 2-adrenoceptor elicited mydriasis. Noradrenergic LC neurons from the cocaine treated and sham sham groups differed significantly in their responsiveness to the inhibitory effects of clonidine (ED50 values micrograms/kg: sham 7.35 +/- 1.13 and cocaine-treated 17.17 +/- 4.40, P less than 0.05). The ED50 values for the mydriatic response were sham 5.71 +/- 0.49 and cocaine-treated 16.42 +/- 0.69 micrograms/kg, respectively, P less than 0.001. No differences in cardiovascular responses to systemically injected clonidine between the chronic cocaine- and sham-treated groups were observed. Chronic cocaine treatment attenuates the two alpha 2-adrenoceptor-mediated responses most likely via an interaction with central catecholaminergic neurotransmission.     

The significance of mydriasis produced by amphetamine sulphate

Summary The mydriatic action of amphetamine on innervated irides appears to be due to both central and peripheral effects of the drug.Thus in intact conscious cats or cat encéphale isolé preparations, the intravenous administration of amphetamine produced considerable pupil dilatation of both innervated and denervated irides. This mydriasis could be abolished or much reduced, particularly for chronic sympathetic denervated irides, by the intravenous injection of central depressant substances such as chloralose or pentobarbitone sodium.In non-anaesthetised spinal, pithed or cerveau isolé cats, the mydriatic action of amphetamine was elicited.In anaesthetised cats, amphetamine dilated the pupil of innervated irides, but in doses unlikely to have any central action, amphetamine had little or no mydriatic action on the chronic sympathetic denervated irides. The mydriatic action of amphetamine could still be obtained after degeneration of the parasympathetic post-ganglionic nerve endings in the iris.The release of catechol amines either directly or reflexly from the adrenal glands in anaesthetised cats is unlikely to contribute significantly to the dilatation of the pupils produced by amphetamine.Impairment of the pupil reflex response to light may follow the intravenous injection of amphetamine, greater doses being required to do this than for the appearance of mydriasis.The relation of these findings to the mydriatic action of some other sympathomimetic amines structurally related to amphetamine, and to the symptoms and signs found in man during intoxication with amphetamine was discussed.     

Central and peripheral components of morphine mydriasis in mice

Mice treated with morphine (intracerebroventricularly, retrobulbarly or intraperitoneally) demonstrated dose related bilateral mydriasis. Intracerebroventricular (ICV) injection was much more potent than either retrobulbar (RB) or intraperitoneal (IP) injections. Morphine applied topically onto one eye resulted in bilateral mydriasis which was more marked in the treated eye. The mydriatic effect was antagonized by naloxone administered either IP or ICV or given on one eye. Here again, ICV naloxone was most effective. Naloxone eye drops diminished the mydriasis produced by systemic morphine bilaterally but more in the treated eye. These results suggest that in mice the mydriasis produced by morphine is mainly of central origin, but a local ocular effect also occurs.     

Intravenous tyramine response in migraine before and during treatment with indoramin.

We studied the response of 31 migraine sufferers (20 women, 11 men) to intravenous tyramine (the tyraminedose)pressor response test). Patients were treated either with pacebo tablets or indoramin, and alpha-adrenergic blocking agent, in a double-blind crrossover trial. We found that patients with migraine required significantly less tyramine to increase their cystolic blod pressure by 30 mm Hg when compared with matched controls. Indoramin significantly increased the amount of tyramine needed to raise the systolic blood pressure among migraine suffers and reduced the incidence of posttyramine migraine for m 46% while patients were on placebo tablets to 8% when they were receiveing indoramin. There was no association between tyramine sensitivity and a history of premenstrual or dietary migraine, nor was there a significant difference in the indierenence in the incidence of post-tyramine migrain between men women. We conclude that the intravenous tyramine test may be valuable in assessing migraine suffers who will respond to an alpha-advenergic blocking agent such as indoramin.     

Mechanism of dexamphetamine-induced mydriasis in the anaesthetized rat.

1. The effect of intravenous administration of dexamphetamine [+)-Amp) on rat pupil diameter was investigated. In all experiments, the vagosympathetic trunks were sectioned bilaterally at the cervical level. 2. In rats anaesthetized with urethane, (+)-Amp (0.1-0.3 mg kg-1, i.v.) produced a dose-related increase in pupil size. The mydriatic effects of (+)-Amp were evident immediately after administration. 3. Pretreatment with the alpha 2-adrenoceptor antagonists yohimbine (1.5 mg kg-1 i.v.) or idazoxan (0.5 mg kg-1, i.v.) blocked the pupillary response to (+)-Amp. Yohimbine caused about a 30 fold shift to the right in the dose-response curve whereas idazoxan almost completely abolished the mydriatic response to (+)-Amp. 4. In contrast, pretreatment with the alpha 1-adrenoceptor antagonist phenoxybenzamine (2 mg kg-1, i.v.), failed to alter significantly the pupillary response to (+)-Amp. 5. Depletion of central nervous system (CNS) monoamines with reserpine (5 mg kg-1, i.p.) and alpha-methyl-p-tyrosine (2 x 300 mg kg-1, i.p.) prevented the pupillary response to (+)-Amp. 6. The mydriatic effect of (+)-Amp was present only in preparations that had intact parasympathetic neural tone to the iris. Central preganglionic denervation of the oculomotor nerve abolished the mydriatic response of (+)-Amp. 7. These results indicate the (+)-Amp acts in the CNS to produce mydriasis in the anaesthetized rat by stimulating CNS postsynaptic alpha 2-adrenoceptors, findings that are consistent with the hypothesis that (+)-Amp acts predominantly as an indirect sympathomimetic agent to release endogenous stores of a monoaminergic neurotransmitter (perhaps noradrenaline).     

Effect of amitraz and chlordimeform on heart rate and pupil diameter in rats: mediated by alpha 2-adrenoreceptors

Pupillary and cardiac responses to the insecticide/acaricide amitraz (0.03 to 1.0 mg/kg, iv) and chlordimeform (0.03 to 10.0 mg/kg, iv), as well as the alpha 2-adrenergic agonists clonidine (1 to 30 micrograms/kg, iv) and xylazine (10 to 300 micrograms/kg, iv), were investigated in rats anesthetized with an ether and pentobarbital combination. Amitraz, clonidine, and xylazine caused a dose-dependent mydriasis and bradycardia. The order of potency of the mydriatic and bradycardic effects was: clonidine greater than xylazine greater than amitraz. Chlordimeform did not cause mydriasis or bradycardia at the dosages studied. Amitraz-induced mydriasis and bradycardia were blocked by antagonists with alpha 2-adrenoreceptor blocking activity: yohimbine and phentolamine (2.5 mg/kg each, iv). In contrast, these effects of amitraz were not affected by prazosin (2.5 mg/kg, iv), an alpha 1-adrenoreceptor antagonist. In rats pretreated with reserpine (7.5 mg/kg, sc, 20 hr) and alpha-methyl-p-tyrosine (250 mg/kg, ip, 5 hr) to deplete catecholamine, amitraz (0.03-1.0 mg/kg, iv) produced mydriasis of similar magnitude as in the control animals. However, amitraz did not lower the heart rate in the pretreated animals as it did in the control animals. The results demonstrated that amitraz, a formamidine, induced mydriasis and bradycardia which were not observed with administration of another formamidine, chlordimeform. The data also suggest that amitraz-induced mydriasis is mediated by postsynaptic alpha 2-adrenoreceptors while amitraz-induced bradycardia is mediated by presynaptic alpha 2-adrenoreceptors.     

托品酰胺与阿托品滴眼液对儿童验光结果的影响比较

目的了解对屈光不正儿童应用托品酰胺或阿托品滴眼液后，散瞳验光及复验结果的符合率。方法186例屈光不正患儿(共372只眼)，均先给予托品酰胺扩瞳，5 min滴眼1次，共3次，最后1次滴药后30 min进行检影验光，并于第2天复验。再嘱患儿自实验第2天复验后开始，用阿托品滴眼液每天滴眼3次，共3 d，第4天复诊时再行验光，并于3周后复验。比较两种药物散瞳验光和复验的结果。结果4～10岁屈光不正儿童远视占多数，～14岁则以近视多见。～14岁近视患儿采用托品酰胺与阿托品散瞳后验光及复验的结果差异无显著性(P＞0.05)，其他患儿采用这两种药物散瞳验光及复验的结果差异有显著性(P＜0.05)。结论托品酰胺是较大年龄(10～14岁)近视性儿童散瞳验光的理想药物，但对其他年龄段儿童和托品酰胺散瞳验光后发现有复性散光的患儿，应使用阿托品。     

Interaction of desipramine and amitriptyline with adrenergic mechanisms in the human iris in vivo

Summary Mydriatic responses of the pupil were evoked by locally instilled noradrenaline and methoxamine in eight healthy volunteers. The effects of three single oral doses (25 mg, 50 mg and 100 mg) of amitriptyline and desipramine were compared on the mydriatic responses. Both antidepressants potentiated the mydriasis evoked by noradrenaline; desipramine appeared to be approximately four times more potent than amitriptyline. Both antidepressants antagonised the mydriasis evoked by methoxamine, amitriptyline being approximately twice as potent as desipramine. It is suggested that the potentiation of the response to noradrenaline may reflect the blockade of the uptake of noradrenaline into adrenergic nerve terminals, whereas the antagonism of the response to methoxamine may reflect the blockade of postsynaptic -adrenoceptors by the antidepressants. It is argued that the interaction of the antidepressants with adrenergic mechanisms could explain why amitriptyline, a potent anticholinergic agent, causes no significant change in resting pupil diameter, while desipramine, a relatively weaker anticholinergic agent, produces a significant mydriasis.     

Factors determining the potency of mydriatic drugs in man.

1 The mydriasis resulting from topical application of five atropine-like drugs was measured photographically in man. Drug potency was obtained from log dose-response curves. 2 The in vitro potency of eight cholinoceptor blocking drugs, including those studied in man, was obtained by measuring their affinity constants for binding to the receptors of an isolated preparation of the rabbit sphincter pupillae. Values agreed closely with those obtained for the muscarinic receptors of guinea-pig ileum. 3 In vitro and in vivo potency was compared to obtain a quantitative measure of the relative ease with which drugs gain access to the receptors after topical application. 4 The large differences that occur in the intensity and duration of the mydriatic response to atropine-like drugs is primarily the result of differences in their ability to blcok the receptors. Only with tropicamide does its relatively high accessibility affect its potency in man.     

Effect of neonatal 6-hydroxydopamine treatment on the blood pressure response to noradrenaline and tyramine in rats

Neonatal treatment of rats with 6-hydroxydopamine (6-OHDA) caused a permanent depletion of noradrenaline (NA) in the heart and the spleen, but not in the adrenals. In 10–12 week old animals, anesthetized with pentobarbital, sensitivity of the pressor response to various doses of i.v. administered NA increased 5-fold whereas the pressor response to i.v. administered tyramine was greatly diminished; the response to tyramine was further reduced after adrenalectomy, but not in controls. These results suggest that the pressor responses evoked by tyramine and NA can be used as a test for functional sympathetic denervation after 6-OHDA treatment.     

Evidence for a central postsynaptic action of clonidine

Summary Intravenous administration of clonidine (1–100 g/kg) produces a dose-dependent mydriasis in cats by inhibition of parasympathetic tone to the iris. The magnitude of CNS-induced pupillary dilation was similar in both normal anaesthetized cats and in araesthetized preparations pretreated with reserpine (5 mg/kg i.p.) and -methyl-p-tyrosine (2×300 mg/kg i.p.). Pretreatment reduced the concentrations of noradrenaline, dopamine and serotonin to less than 3% of that control levels in most parts of the CNS in which these amines were measured. Clonidine produced bradycardia in control animals but not in pretreated cats. In amine depleted animals in which only one eye was innervated by the ciliary nerves (parasympathetic), clonidine produced mydriasis only on the innervated side.These experiments confirm our previous observations that clonidine produces mydriasis in the cat by means of inhibition of parasympathetic tone to the iris. It is concluded that if clonidine produces this effect by stimulating noradrenergic, dopaminergic or serotonergic receptors, then clonidine exerts its centrally-induced mydriatic effect by acting on post-synaptic mechanisms.     

Microsomal enzymes and potentiation of tyramine pressor response

Therapy with monoamine oxidase (MAO) inhibitors has produced hypertensive crises in patients who have ingested tyramine in food. This effect has been attributed to the inability of inhibited MAO to degrade tyramine, but recent work suggests that inhibition of hepatic microsomal oxidative enzymes may also be involved. In our experiments, SKF-525A was more potent (1000 times) than phenelzine as an inhibitor of microsomal tyramine hydroxylase, but less potent than phenelzine in potentiating the pressor response of tyramine. As SKF-525A was also shown to inhibit MAO (10 times less potent than phenelzine), it is suggested that inhibition of tyramine hydroxylase is not a major factor in potentiating the pressor response. In animals in which the microsomal enzymes were induced with phenobarbital, the pressor response to tyramine was not reduced, as would be expected if microsomal enzymes were regulating tyramine levels. These experiments suggest that tyramine potentiation is probably not a problem in therapy with drugs known to be microsomal enzyme inhibitors if these drugs have no MAO inhibitory activity.     

Pharmacodynamics of a new ophthalmic mydriatic insert in healthy volunteers: potential alternative as drug delivery system prior to cataract surgery

Cataract surgery requires a satisfactory degree of mydriasis throughout the entire operation. A phase I, open-labelled, randomised, cross-over trial was conducted in 18 healthy volunteers to compare mydriasis obtained with subsequent administration of phenylephrine 10% and tropicamide 0.5% eyedrops or a new insoluble-matrix retropalpebral ophthalmic insert containing 5.38 mg phenylephrine and 0.28 mg tropicamide. Phenylephrine serum concentrations were measured over 6 hr following each treatment administration. Secondary end-points included cardiovascular, general and local tolerance and quantification of bacterial colonisation of the conjunctiva and the cultured insert, respectively. When normalized to the pupil diameter after conventional treatment, the diameter achieved with the insert was 1.13 (95% confidence interval, 0.94-1.48, P=0.38). Moreover, standard eye drops provided faster effective mydriasis than the insert, starting 30 min. as compared to 90 min. upon treatment administration (P<0.01, repeated-measures ANOVA). Phenylephrine concentrations remained almost undetectable for both treatments and no change in heart rate or blood pressure were observed throughout the study. Only three superficial punctuate keratitis were diagnosed with the insert and two with the eye drops. No significant bacterial contamination of conjunctiva swab and cultured insert was observed. The new insoluble-matrix retropalpebral ophthalmic mydriatic insert produced similar but delayed effective and prolonged mydriasis as compared to the standard delivery system. In addition to its potential usefulness in patients undergoing cataract surgery, such new ophthalmic delivery system may be an advantage in children who need to undergo fundus photography due to the single administration and excellent tolerance as well.     

樟柳碱的扩瞳与调节麻痹作用

目的：观察樟柳碱眼药水对人眼的扩瞳作用与调节麻痹作用。方法：３０例观察对象（男性２２例，女性８例；年龄１６±ｓ５ａ）均一眼滴用０．２％樟柳碱眼药水，另一眼作空白对照；观察扩瞳作用，用调节卡测定剩余调节力。结果：瞳孔扩至最大时间为４５±５ｍｉｎ，瞳孔恢复正常时间为７５±４ｈ；在药物作用高峰期，剩余调节力为１．７±０．５Ｄ。结论：樟柳碱的扩瞳与调节麻痹作用有临床应用价值；樟柳碱眼药水的应用是安全的