Hydroxyamphetamine mydriasis in normal subjects and hydroxyamphetamine mydriasis in Horner's syndrome.
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Horner Syndrome↗
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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 micrograms) 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 x 10 microliters), and in the last two sessions (Experiment 2) the effect of clonidine or placebo on the mydriasis to methoxamine hydrochloride eyedrops (20 mM; 2 x 10 microliters) 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 micrograms) 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.
Adolescent↗
Mediation of mydriasis in conscious rats by central postsynaptic alpha 2-adrenoceptors.
The alpha 2-adrenoceptor agonist, clonidine (0.001-1 mg/kg, IP), dose-dependently induced mydriasis in conscious rats (ED50 0.088 mg/kg). This response was maximal when measured 10 min after clonidine injection and was of about 30-min duration. The noradrenaline releasing agent, methamphetamine (0.75 mg/kg, IP), also increased pupil diameter. Clonidine (0.03 mg/kg, IP)-induced mydriasis was inhibited in a dose-related fashion by the alpha 2-adrenoceptor antagonists, idazoxan (0.03-3 mg/kg, IP) and yohimbine (0.03-3 mg/kg, IP), but was unaltered by the alpha 1- or beta-adrenergic antagonists, prazosin (1 and 3 mg/kg, IP) or pindolol (1 and 3 mg/kg, IP). Methamphetamine (0.75 mg/kg, IP)-induced mydriasis was similarly inhibited by idazoxan (1 mg/kg, IP) and yohimbine (1 mg/kg, IP). These data argued strongly that central alpha 2-adrenoceptors are involved in the mediation of mydriasis. The synaptic location of these receptors was determined using DSP-4 (50 mg/kg x 2, IP) to lesion noradrenergic neurones: this produced a 64% depletion of noradrenaline in the midbrain (containing the Edinger-Westphal nucleus responsible for mydriasis) and reduced the mydriatic effect of methamphetamine (0.75 mg/kg, IP) to a similar extent (72%), whereas clonidine mydriasis remained unaltered. Therefore, these results show that the mydriasis responses induced by either clonidine or methamphetamine are mediated by central postsynaptic alpha 2-adrenoceptors.
Adrenergic Agents↗
Clonidine-induced hypoactivity and mydriasis in mice are respectively mediated via pre- and postsynaptic alpha 2-adrenoceptors in the brain.
Since brain alpha 2-adrenoceptors occur both pre- and postsynaptically, experiments were carried out to determine the synaptic locations of those receptors mediating clonidine-induced hypoactivity and mydriasis. Intraperitoneal (i.p.) injection of clonidine (1-3000 micrograms/kg) to mice dose dependently induced these two responses and also decreased brain concentrations of 3-methoxy-4-hydroxyphenylglycol (MHPG). The ED50 values were: 120 micrograms/kg for hypoactivity (95% confidence limits 103-140 micrograms/kg), 54 micrograms/kg for mydriasis (95% confidence limits 40-74 micrograms/kg) and 18 micrograms/kg for MHPG reduction (95% confidence limits 8-36 micrograms/kg) suggesting that these responses could all be presynaptically mediated. However, methamphetamine which increases noradrenaline turnover was found to dose dependently produce mydriasis, but not hypoactivity, after peripheral (0.1-5 mg/kg i.p.) or central (0.5-10 micrograms i.c.v.) injection. The mydriasis produced by methamphetamine (0.5 mg/kg i.p.) was abolished by i.c.v. injection of 1 micrograms idazoxan or yohimbine, but not 2.5 micrograms prazosin or pindolol, showing this effect was mediated by central alpha 2-adrenoceptors. Methamphetamine (1-10 micrograms i.c.v.) potentiated the mydriasis induced by clonidine (50 micrograms/kg i.p.) suggesting this was a postsynaptic alpha 2-adrenoceptor response. By contrast, methamphetamine (1-10 micrograms i.c.v.) dose dependently reversed clonidine (100 micrograms/kg i.p.) hypoactivity indicating this response was mediated by presynaptic alpha 2-adrenoceptors. These hypotheses were confirmed by destruction of noradrenergic neurones using DSP-4 (100 mg/kg i.p. x 2). This treatment prevented the mydriasis response to methamphetamine (0.5 mg/kg i.p.), but not clonidine (100 micrograms/kg i.p.) and markedly attenuated clonidine (100 micrograms/kg i.p.) hypoactivity.
Animals↗
Effect of mydriasis on visual field area in retinitis pigmentosa.
PURPOSE: The effect of mydriasis on Goldmann visual field area in patients with retinitis pigmentosa has not been suitably defined. The aim of this study is to determine whether visual field area in these patients varies with pharmacologic mydriasis. METHODS: Fifteen adult patients with retinitis pigmentosa were studied prospectively. Goldmann visual fields with II4e and V4e isopters were obtained in both eyes before and after full pharmacologic mydriasis of the right eye. The isopter areas were quantified and analyzed to determine the effect of mydriasis on visual field area. RESULTS: The difference in the right eye isopter areas was compared with the difference in the left eye isopter areas using paired t tests, where the differences were computed from areas obtained before and after dilation of the right eye. Mydriasis had no significant effect on the visual field in terms of isopter area difference (II4e, P = 0.87; V4e, P = 0.45) and percent change in isopter area (II4e, P = 0.81; V4e, P = 0.24). CONCLUSION: Pharmacologic mydriasis had no appreciable effect on the Goldmann visual field area in a selected group of patients with retinitis pigmentosa. These findings suggest that visual fields of such patients obtained in the dilated or undilated state can be meaningfully compared.
Adult↗
Pilocarpine mydriasis in mice.
In several rodent species pilocarpine and oxotremorine produce mydriasis, rather than the miosis which is characteristic of most other species. We have established that pilocarpine is a mydriatic drug in mice, a species in which the action has previously not been described, and that this effect occurs after local ocular, intraperitoneal (IP) or intracerebroventricular (ICV) application. Arecoline produces miosis or mydriasis (depending on dose) following direct ocular application but mild mydriasis after IP or ICV injection. Atropine also produces mydriasis in mice, and the effect of pilocarpine is additive with that produced by atropine and is not antagonized by antihistamines. Direct ICV pilocarpine injection produces mydriasis at doses equivalent to those used systemically. Pilocarpine mydriasis probably results from inhibition of parasympathetic activity.
Animals↗
Clonidine produces mydriasis in conscious mice by activating central alpha 2-adrenoceptors.
Intraperitoneal (i.p.) injection of the alpha 2-adrenoceptor agonist clonidine (1-3000 micrograms/kg) produced dose-dependent pupil dilatation in conscious C57/Bl/6 mice with an ED50 of 54 micrograms/kg (95% confidence limits 40-74 micrograms/kg). This response was rapid in onset and of approximately 30 min duration. The alpha 2-adrenoceptor antagonists idazoxan (1 or 3 mg/kg i.p.) and yohimbine (1 or 3 mg/kg i.p.) both produced dose-related miosis, but the alpha 1- and beta-adrenoceptor antagonists prazosin (1 or 3 mg/kg i.p.) and pindolol (1 or 3 mg/kg i.p.) were without effect. These doses of idazoxan and yohimbine potently reversed the mydriasis induced by clonidine (100 micrograms/kg i.p.), while prazosin and pindolol were again ineffective. Clonidine-induced mydriasis was also unaltered by the 5-HT antagonists, methysergide (2.5 mg/kg i.p.) and ketanserin (0.1 mg/kg i.p.) or 0.1 mg/kg i.p. of the dopamine antagonists, haloperidol, SCH 23390 and BRL 34778. A dose of 0.25 microgram clonidine, which was ineffective when administered i.p., produced marked mydriasis after intracerebroventricular (i.c.v.) injection. In addition, the mydriasis produced by i.p. injection of clonidine (100 micrograms/kg) was abolished by i.c.v. dosing of 2.5 micrograms idazoxan or yohimbine, but again not by prazosin or pindolol. Together, these data provide strong evidence to indicate that clonidine-induced mydriasis is exclusively mediated via central alpha 2-adrenoceptors and that this response provides a useful model for studying the function of these receptors.
Adrenergic alpha-Agonists↗
alpha 2-Adrenoceptor agonists induced mydriasis in the rat by an action within the central nervous system.
1 The effects of intravenous administration of the selective alpha 2-adrenoceptor agonists clonidine, UK 14,304 and guanoxabenz on rat pupil diameter were investigated. 2 In rats anaesthetized with pentobarbitone, each agonist produced a marked dose-related increase in pupil diameter; the rank order of potency was: clonidine greater than UK 14,304 greater than guanoxabenz. 3 Pretreatment with the selective alpha 2-adrenoceptor antagonist, RX 781094 (0.5 mg/kg, i.v.), produced a parallel 30-40 fold shift to the right of the dose-pupil dilator response curves for the three agonists. Yohimbine (1.5 mg/kg, i.v.) produced about a 10 fold rightward shift of the dose-response curve for guanoxabenz. In contrast, the alpha 1-selective antagonist, prazosin (0.5 mg/kg, i.v.), failed to affect the dose-response relation for guanoxabenz. 4 Several antagonists of varying selectivities towards alpha 1- and alpha 2-adrenoceptors were tested for their ability to reverse the maximal mydriasis induced by guanoxabenz (0.3 mg/kg, i.v.). The rank order of potency of the antagonists producing a 50% reversal of this effect was: RX 781094 greater than yohimbine greater than piperoxan = rauwolscine greater than mianserin greater than RS 21361. Neither corynanthine nor prazosin reversed the guanoxabenz-induced mydriasis. 5 Topical application of RX 781094 (0.1 to 3% w/v solutions) onto one eye produced a slow reversal of guanoxabenz-induced mydriasis; the time course and degree of reversal were virtually the same in both eyes. 6 Intracerebroventricular administration of RX 781094 (1.25-15 micrograms total dose) caused a rapid dose-related reversal of the maximal mydriasis induced by guanoxabenz (0.3 mg/kg, i.v.). 7 Guanoxabenz (0.3 and 1.0 mg/kg, i.v.) did not produce any dilation of the physostigmine-constricted undamaged pupil of the pithed rat. Intravenous adrenaline was found to produce a small mydriatic effect, while atropine completely antagonized the effects of physostigmine in this preparation. 8 These results indicate that alpha 2-adrenoceptor agonists induce mydriasis in the rat through a central alpha 2-adrenoceptor mechanism. However, the site of action within the central nervous system remains to be determined.
Adrenergic alpha-Agonists↗
Mechanism of morphine-induced mydriasis in the cat.
Neurons that increased their firing rate in response to light stimulation were recorded from the pretectal region and the anterior oculomotor nucleus of sedated immobilized cats while morphine (2 mg/kg iv) was administered. The dose produced mydriasis and an increase in spontaneous firing rate of all light-sensitive neurons recorded from the anterior oculomotor nucleus. This suggested that morphine did not produce mydriasis through inhibition of the third nerve. Phenoxybenzamine, iv or topically, antagonized the mydriasis, indicating a peripheral source of sympathetic input as the basis for morphine-induced mydriasis. Morphine (2 mg/kg iv), administered 1 h after adrenalectomy, produced miosis and increased the spontaneous firing rate of light-sensitive neurons recorded from the oculomotor nucleus. These observations suggest that, in the cat, although morphine activates the oculomotor neurons to produce miosis, the effect is masked by the morphine-induced release of catecholamines, mainly from the adrenal glands, which produced mydriasis.
Action Potentials↗
Comparison of prednisolone acetate and indomethacin for maintaining mydriasis during cataract surgery.
Preoperative topical nonsteroidal anti-inflammatory drugs such as flurbiprofen and indomethacin have been found to maintain mydriasis during cataract surgery. Steroidal anti-inflammatory drugs are commonly used to treat postoperative inflammation, but their effect on the maintenance of intraoperative mydriasis is unknown. Forty-six patients admitted for elective cataract surgery were randomly assigned to one of three treatment groups and received 1% prednisolone acetate, 1% indomethacin or artificial tears four times before surgery, in addition to standardized preoperative dilating drops and intraoperative epinephrine. Pupillary diameter was measured and the time interval noted five times during the surgery. During surgery the indomethacin group lost significantly less mydriasis than the control group. The mydriasis losses of the prednisolone acetate group were between those of the indomethacin and control groups, but these differences did not reach significance. We conclude that prednisolone acetate is less effective than indomethacin for maintaining mydriasis during cataract surgery.
Adult↗
Unilateral mydriasis after induction of anaesthesia.
Unilateral mydriasis is a disturbing finding during anaesthesia and may indicate serious neurological injury. In addition, the assessment of abnormal neurological findings is limited during general anaesthesia, and therefore requires special consideration. I report finding a dilated right pupil (7 mm, nonreactive to light) after bronchoscopic tracheal intubation and induction of general anaesthesia in a frail, 74-yr-old woman with cervical subluxations and spinal cord impingement. The possible aetiology of the unilateral mydriasis includes the effects of anaesthetic agents, stellate ganglion block, impaired venous return from the head and neck, acute intracranial mass lesion or an haemorrhagic event, direct eye trauma, pre-existing medical or surgical conditions, and inadvertent direct deposition of alpha-adrenergic or anticholinergic agents in the eye. Consideration of these factors, the autonomic innervation of the eye, and an intraoperative "wake-up" test allowed satisfactory neurological assessment in this patient and surgery to proceed. Unilateral mydriasis, while unusual, may be seen during general anaesthesia and requires thorough knowledge of autonomic nerve pathways and pharmacology of the eye for correct diagnosis. In this case, mydriasis was considered to result from phenylephrine/lidocaine spray which was used to provide topical anaesthesia to the airway.
Aged↗
Amaurotic mydriasis.
Amaurotic mydriasis is characterized by larger than normal pupils in patients with visual loss. In sought to establish whether amaurotic mydriasis can reliably identify different kinds of visual loss and whether this static measurement might prove useful in discerning "balanced" bilateral optic neuropathies where no relative afferent pupillary defect (RAPD) is detected. Patients with binocular pregeniculate visual loss, patients with balanced binocular pregeniculate loss without RAPD, and patients with monocular pregeniculate visual loss had significantly larger pupils than age-matched controls. Although pupils of patients with binocular pregeniculate visual loss (20/50 or better in one or both eyes) were significantly smaller than pupils of age-matched patients with binocular pregeniculate deficits of worse than 20/50 in one or both eyes, no such correlation between Snellen visual acuity and amaurotic mydriasis was found in patients with monocular pregeniculate visual loss. Amaurotic mydriasis is a clinically useful phenomenon that may identify pregeniculate disease in the absence of a RAPD or distinguish pregeniculate from postgeniculate visual loss.
Blindness↗
Clonidine mydriasis in the rat.
Pupillary responses to clonidine (3--100 micrograms/kg, i.v.) and epinephrine (1--30 micrograms/kg, i.v.) were observed in anesthetized rats. Clonidine caused a dose-dependent mydriasis which was effectively antagonized by pretreatment with yohimbine (1.5 mg/kg, i.v.). Pretreatment with phentolamine (5 mg/kg, i.v.) was less effective in antagonizing this clonidine-induced mydriasis. Phenoxybenzamine (2 mg/kg, i.v.) was almost without effect. In contrast, both phentolamine and phenoxybenzamine blocked the pupillary dilation produced by epinephrine while yohimbine pretreatment resulted in no antagonism of epinephrine-induced mydriasis. These results suggest that clonidine-induced mydriasis in the rat is mediated by a central adrenergic inhibitory mechanism.
Adrenergic alpha-Antagonists↗
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.
Animals↗
Effective degree of mydriasis with phenylephrine and tropicamide.
The mydriatic effects of several concentrations of phenylephrine and of tropicamide were studied in 84 young adults for 90 min following topical instillation. Pupillary diameter was estimated (a) under ambient photopic illumination and (b) when illumination was increased to that associated with direct ophthalmoscopy. Evaluation was made of the "degree of mydriasis," i.e., the difference in pupillary diameter between the eye receiving the mydriatic agent and the contralateral control eye when the pupillary light reflex was stimulated. In subjects with light or hazel irides, phenylephrine caused maximal dilatation in 60 to 75 min, mean values being 5.6 mm with 1 drop of 2%, 6.0 mm with 2 drops of 2.5%, and 7.1 mm with 1 drop of 10%. Maxiumum degrees of mydriasis were 3.0 mm with 2 drops of 2.5% and 3.1 mm with 1 drop of 10%. With 0.5% tropicamide, maximum diameter was 8.0 mm in 30 min in subjects with light, hazel, or brown irides, and the maximum degree of mydriasis was 5.0 mm. It is concluded that when a mydriatic agent is used to facilitate intraocular visualization, neither specification in terms of (a) maximum diameter under ambient illumination nor (b) degree of mydriasis provides optimal characterization. It is suggested that the "clinically effective diameter," i.e., pupillary diameter under illumination corresponding to that to be used during examination, would be the most useful specification.
Adaptation, Ocular↗
Xylazine-induced mydriasis in rats and its antagonism by alpha-adrenergic blocking agents.
Pupillary response to xylazine (10-300 micrograms/kg, i.v.) norepinephrine (1-30 micrograms/kg. i.v.) and atropine (3-100 micrograms/kg, i.v.) were observed in rats anaesthetized with pentobarbital. Xylazine caused a dose-dependent mydriasis which was antagonized by a selective alpha 2-adrenergic blocking agent, yohimbine (2.5 mg/kg, i.v.). was less effective in antagonizing this effect of xylazine. A selective alpha 1-adrenergic blocking agent, prazosin (2.5 mg/kg, i.v.) was ineffective in reducing the xylazine-induced mydriasis. In contrast, both phentolamine and prazosin blocked the pupillary dilation produced by norepinephrine, while yohimbine was much less effective in antagonizing norepinephrine-induced mydriasis. Atropine also induced a dose-dependent mydriasis which was not affected by yohimbine pretreatment. The present study suggests that the mydriatic effect of xylazine in the rat is mediated by an adrenergic mechanism, possibly by stimulating the alpha 2-adrenergic receptors in the iris and CNS.
Adrenergic alpha-Antagonists↗
Xylazine-induced mydriasis: possible involvement of a central postsynaptic regulation of parasympathetic tone.
Intravenous injection of xylazine (0.01-1 mg/kg) produced a dose-dependent mydriasis associated with a depression of tonic ciliary nerve activity in anesthetized cats. Xylazine-induced mydriasis was apparent in the sympathectomized iris but was absent in the parasympathectomized, physostigmine-treated iris. Epinephrine (30 micrograms/kg, i.v.) produced a slightly greater mydriasis in the sympathectomized iris than in the parasympathectomized, physostigmine-treated iris. The alpha 2-adrenergic blocking agent, yohimbine (0.5 mg/kg, i.v.) antagonized the pupillary dilation and reversed the depression of ciliary nerve activity induced by xylazine administration. In rats pretreated with reserpine (7.5 mg/kg, s.c., 20 h) and alpha-methyl-p-tyrosine (250 mg/kg, i.p., 5 h), intravenous injection of xylazine (0.01-1 mg/kg) resulted in mydriasis of similar magnitude as control animals. However, xylazine induced bradycardia in the control group but not in the pretreated animals. The results suggest that pupillary dilation produced by i.v. xylazine is primarily the result of a central inhibition of parasympathetic tone to the iris. It also appears that xylazine produces this effect via postsynaptic alpha 2-adrenergic mechanisms, while it produces bradycardia through a presynaptic alpha 2-adrenergic mechanism.
Animals↗
Role of sympathetic system in morphine-induced mydriasis in rat.
The effects of three doses (5, 30, and 60 mg/kg) of morphine on pupillary diameter (PD) were studied in rats that were either normal, neurotransmitter antagonist pretreated, guanethidine pretreated, cervical sympathectomized, or adrenalectomized. Morphine produced a dose-dependent increase in PD and exophthalmos. In addition, the PD concurrently underwent fluctuations. alpha-Adrenergic antagonists blocked both mydriasis and exophthalmos, whereas a beta-adrenergic antagonist had no significant effect. This suggested a role for the sympathetic nervous system. However, cervical sympathectomy or guanethidine pretreatment only partially blocked the increase in PD or exophthalmos. Adrenalectomy also partially blocked the mydriasis and exophthalmos. Adrenalectomy combined with guanethidine pretreatment completely blocked morphine-induced mydriasis but no exophthalmos. Thus, the results suggest that both direct sympathetic innervation and hormonal action from the adrenals are involved in morphine-induced mydriasis in the rat.
Adrenalectomy↗