Effects of topical antiglaucoma eye drops on prostaglandin E(2)-induced aqueous flare elevation in pigmented rabbits

PURPOSE: To evaluate the role of topical instillation of some antiglaucoma agents on experimental elevation of aqueous flare induced by prostaglandin E(2) (PGE(2)) in pigmented rabbits. METHODS: Transcorneal diffusion of PGE(2) (25 microg/mL or 7.09 x 10(-2) mM) with the use of a glass cylinder was achieved to produce aqueous flare elevation in pigmented rabbits. An antiglaucoma agent was topically administered before application of PGE(2). Aqueous flare was measured with a laser flare cell meter. RESULTS: A single instillation of apraclonidine 1.15%, two instillations of epinephrine 1.25%, two instillations of dipivefrin 0.1%, and two instillations and one instillation of dipivefrin 0.04% eye drops inhibited 98%, 96%, 87%, 73%, and 47% of PGE(2)-induced aqueous flare elevation, respectively. Timolol 0.5%, nipradilol 0.25%, dorzolamide 1%, and pilocarpine 2% eye drops had no effects on the increase of PGE(2)-induced flare. CONCLUSIONS: Apraclonidine, epinephrine, and dipivefrin eye drops inhibit PGE(2)-induced elevation of aqueous flare in pigmented rabbits.     

Effects of topical corticosteroids and nonsteroidal anti-inflammatory drugs on prostaglandin e2-induced aqueous flare elevation in pigmented rabbits

We evaluated the effects of anti-inflammatory potency of corticosteroids and nonsteroidal anti-inflammatory drugs on prostaglandin E2 (PGE2)-induced aqueous flare elevation in pigmented rabbits. Transcorneal diffusion of PGE2, 25 microg/ml (7.09 x 10(-2) mmol/l), with the use of a glass cylinder was achieved to produce aqueous flare elevation. Anti-inflammatory drugs were topically administered once before PGE2 application. Aqueous flare was measured with a laser flare-cell meter. Topical single instillation of dexamethasone sodium metasulfobenzoate 0.1%, dexamethasone sodium phosphate 0.1%, and fluorometholone 0.1% 6 h before PGE2 application inhibited 56, 59, and 43% of flare elevation, respectively. Topical single instillation of bromfenac sodium 0.1% and pranoprofen 0.1% 1 h before PGE2 application inhibited 33 and 15% of flare elevation, respectively. Indomethacin 0.5% did not inhibit flare elevation. Corticosteroid eyedrops needed several hours from topical instillation to exhibit inhibition of flare elevation. Most nonsteroidal anti-inflammatory drug eyedrops inhibited aqueous flare elevation when instilled 1 h before PGE2 application.     

Effects of intravenous administration of FR122047 (a selective cyclooxygenase 1 inhibitor) and FR188582 (a selective cyclooxygenase 2 inhibitor) on prostaglandin-E2-induced aqueous flare elevation in pigmented rabbits

PURPOSE: Two isoforms of cyclooxygenase (COX-1 and COX-2) exist. To determine in vivo effects of the intravenous administration of FR122047 (a selective COX-1 inhibitor), FR188582 (a selective COX-2 inhibitor), diclofenac sodium or dexamethasone phosphate disodium on prostaglandin-E2 (PGE2)-induced aqueous flare elevation and mRNA levels for COX-1 and COX-2 in pigmented rabbits. METHODS: To produce aqueous flare elevation in rabbits, PGE2, 25 microg/ml, was applied to the cornea with the use of a glass cylinder. FR122047, FR188582, diclofenac sodium or dexamethasone phosphate disodium was intravenously injected before PGE2 application. Aqueous flare was measured with a laser flare-cell meter. The mRNA levels for COX-1 and COX-2 in the iris-ciliary body were determined by real-time polymerase chain reaction. RESULTS: FR122047, FR188582 and diclofenac sodium (15 micromol/kg each) injected intravenously 30 min before PGE2 application inhibited 29 +/- 5, 40 +/- 12 and 50 +/- 9% of aqueous flare elevation, respectively. Simultaneous injection of FR122047 (15 micromol/kg) and FR188582 (15 micromol/kg) 30 min before PGE2 application inhibited 61 +/- 8% of flare elevation. Dexamethasone phosphate disodium (15 micromol/kg) injected intravenously 300 min before PGE2 application inhibited 68 +/- 8% of aqueous flare elevation. Less than 3-fold changes in mRNA levels for COX-1 and COX-2 in the iris-ciliary body were noted after PGE2, FR122047, FR188582, diclofenac sodium or dexamethasone phosphate disodium treatment. CONCLUSION: It is possible that enzyme activities of both COX-1 and COX-2 may be involved in the mechanism of PGE2-induced aqueous flare elevation in pigmented rabbits.     

Effects of scutellariae radix extract and its components (baicalein, baicalin, and wogonin) on the experimental elevation of aqueous flare in pigmented rabbits

PURPOSE: To evaluate the possible inhibitory effects of hot water extract of Scutellariae radix and its major components (baicalein, baicalin, and wogonin) on experimental elevation of aqueous flare in pigmented rabbits. METHODS: To produce aqueous flare elevation in rabbits, prostaglandin E(2) (PGE(2)), 25 microg/mL, was applied to the cornea with the use of a glass cylinder, or lipopolysaccharides (LPS), 0.5 microg/kg, were injected into an ear vein. Animals were pretreated by the oral administration of 150 g/day of food containing 0.02%, 0.07%, or 0.2% (w/w) extract of Scutellariae radix for 5 days, or by intravenous injection of baicalein, baicalin, or wogonin, 60 microg/kg or 600 microg/kg, 30 minutes before experimental uveitis was induced. Aqueous flare was measured with a laser flare-cell meter. Aqueous flare intensity was expressed as the area under the curve (AUC) in arbitrary units. RESULTS: The AUC of PGE(2)- and LPS-induced aqueous flare elevation was 1,343 and 5,066 arbitrary units, respectively. Pretreatment by oral administration of 0.07% or 0.2% extract of Scutellariae radix did not inhibit PGE(2)-induced aqueous flare elevation (AUC: 1,252 and 1,210, respectively), but it did inhibit LPS-induced aqueous flare elevation (AUC: 2,248 and 1,973, respectively). Pretreatment by intravenous injection of 600 microg/kg of baicalein, baicalin, or wogonin inhibited LPS-induced aqueous flare elevation (AUC: 2,289, 2,163, and 1,509, respectively). Pretreatment with 60 microg/kg of wogonin also inhibited LPS-induced aqueous flare elevation (AUC: 1,980). CONCLUSION: Hot water extract of Scutellariae radix may have an inhibitory effect on experimental anterior uveitis induced by LPS in pigmented rabbits.     

Effect of topical betaxolol on acute rise of aqueous flare induced by prostaglandin E(2) in pigmented rabbits.

PURPOSE: To evaluate the effects of topical betaxolol on experimental ocular inflammation. METHODS: Transcorneal diffusion of 25 microg/mL (7.09 x 10(-2) mmol/L) of prostaglandin E(2) (PGE(2)), placed in a glass cylinder, was employed to induce aqueous flare elevation in pigmented rabbits. Betaxolol was administered topically before PGE(2) application. Aqueous flare was measured with a laser flare cell meter. RESULTS: Four-, two-, and one-time topical instillations of betaxolol inhibited the PGE(2)-induced aqueous flare elevation by 44% +/- 8%, 32 +/- 7%, and 8 +/- 6%(mean +/- SD), respectively. The inhibition of flare elevation was dependent on the number of betaxolol instillations. CONCLUSION: Topical betaxolol has an inhibitory effect on PGE(2)-induced aqueous flare elevation in rabbit eyes.     

Effect of topical iganidipine on experimental elevation of aqueous flare induced by prostaglandin E(2) and EP agonists in pigmented rabbits

We evaluated the role of topical iganidipine on experimental aqueous flare elevation in rabbits. Transcorneal diffusion of prostaglandin E(2) (PGE(2)), 25 microg/ml or 7.09 x 10(-2) mmol/l, or highly selective agonists for prostaglandin E(2) receptor subtypes (EP), 25 microg/ml, was achieved with the use of a glass cylinder to produce aqueous flare elevation in pigmented rabbits. Iganidipine was topically administered before application of PGE(2) or EP agonists. Aqueous flare was measured with a laser flare cell meter. Topical instillation of 0.1% iganidipine once or twice inhibited 64 +/- 8% (p < 0.01) and 84 +/- 9% (p < 0.01) of PGE(2)-induced aqueous flare elevation, respectively. Two instillations of 0.1% iganidipine inhibited 95 +/- 5% (p < 0.01) of EP2-agonist(ONO-AE1-259-01)-induced flare elevation and 98 +/- 3% (p < 0.01) of EP4-agonist(ONO-AE1-392)-induced flare rise. Topical iganidipine may have anti-inflammatory activity in the eye.     

Effects of isopropyl unoprostone, latanoprost, and prostaglandin E(2) on acute rise of aqueous flare in pigmented rabbits

PURPOSE: To evaluate the effect of isopropyl unoprostone, latanoprost, and prostaglandin E(2) (PGE(2)) on aqueous flare elevation. METHODS: Isopropyl unoprostone (0.12%) or latanoprost (0.005%) was topically instilled. Transcorneal diffusion of PGE(2), 25 microg/ml, using a glass cylinder, was achieved in pigmented rabbits. Aqueous flare was measured with a laser flare cell meter. RESULTS: Topical instillation of isopropyl unoprostone induced aqueous flare elevation in rabbit eyes. Also, topical isopropyl unoprostone additionally induced aqueous flare elevation in eyes with transcorneal diffusion of PGE(2). Latanoprost did not induce flare elevation. CONCLUSION: Isopropyl unoprostone induced aqueous flare elevation in rabbits, and latanoprost did not produce aqueous flare elevation.     

Effect of topical betaxolol on the acute rise of aqueous flare induced by highly selective agonists for prostaglandin E2 receptor subtypes in pigmented rabbits

PURPOSE: To evaluate the role of topical betaxolol on experimental ocular inflammation in rabbits. METHOD: Transcorneal diffusion of highly selective agonists for prostaglandin E2 receptor subtypes (EP), 25 microg/ml, with the use of a glass cylinder, was performed to produce aqueous flare elevation in pigmented rabbits. Betaxolol was topically administered before EP agonist application. Aqueous flare was measured with a laser flare cell meter. RESULTS: Performing topical instillation of 0.5% betaxolol 4 times inhibited 52 +/- 9% of EP2-agonist (ONO-AE1-259-01)-induced aqueous flare elevation. The inhibition of flare elevation was dependent on the number of betaxolol instillations. Betaxolol did not suppress the elevation induced by an EP4 agonist (ONO-AE1-392). CONCLUSION: Betaxolol inhibited EP2-agonist-induced aqueous flare elevation in pigmented rabbits.     

Effects of topical clonidine on prostaglandin-E(2)-induced aqueous flare elevation in pigmented rabbits

We evaluated the role of topical clonidine on experimental ocular inflammation. Transcorneal diffusion of prostaglandin (PG) E(2), 7. 09 x 10(-2) mmol/l, with the use of a glass cylinder was employed to produce aqueous flare elevation in pigmented rabbits. Clonidine was topically administered and yohimbine was injected intravenously. Aqueous flare was measured with a laser flare cell meter. Topical instillation of 0.25% clonidine inhibited 89% of PGE(2)-induced aqueous flare elevation. Instillation of clonidine at 60 or 30 min before and 10 min after PGE(2) inhibited flare significantly. Pretreatment with intravenous yohimbine decreased the clonidine-induced inhibition of the flare elevation in a dose-dependent manner. It is possible that the anti-inflammatory action of topical clonidine may be mediated partly by alpha(2)-receptors.     

Effects of Kakkon-to and Sairei-to on experimental elevation of aqueous flare in pigmented rabbits.

PURPOSE: To evaluate the possible inhibitory effects of Kakkon-to and Sairei-to, traditional Sino-Japanese herbal medicines, on experimental aqueous flare elevation in pigmented rabbits. METHODS: Anterior uveitis was induced either by an application of prostaglandin E2 (PGE2), 10 microg/mL, to the cornea, or an intravenous injection of lipopolysaccharides (LPS), 0.5 microg/kg, in an ear vein. Dose dependency of experimental uveitis induced by LPS (0.1, 0.25, 0.5, or 1.0 microg/kg) was also determined. For pretreatment, about 150 g/day of food containing Kakkon-to (1% w/w) or Sairei-to (0.6% or 2% w/w) was given to two groups of animals for 5 days before experimental uveitis was induced. A third group of animals underwent pretreatment with betamethasone, 130 microg/kg, injection into an ear vein 4 hours before experimental uveitis was induced. A fourth group of rabbits with no herbal medicine or betamethasone pretreatment served as controls. Aqueous flare was measured using a laser flare-cell meter. Aqueous flare intensity was expressed as the area under the curve (AUC) in arbitrary units. RESULTS: The increase in aqueous flare induced by LPS was dose-dependent. The AUC of PGE2 (10 microg/mL) and LPS (0.5 microg/mL) induced aqueous flare elevations were 1,119 and 4,950 arbitrary units, respectively. Kakkon-to (AUC, 1,055) and Sairei-to (AUC, 965) did not inhibit the aqueous flare elevation induced by PGE2. Beta-methasone did inhibit the elevation (AUC, 271). Kakkon-to (AUC, 4,495) did not suppress the aqueous flare elevation induced by LPS. Both 0.6% and 2% Sairei-to (AUC, 2,478, and 978) and beta-methasone (AUC, 443) did suppress the aqueous flare elevation induced by LPS significantly (P < .05). CONCLUSION: Sairei-to could have an inhibitory effect on experimental anterior uveitis induced by LPS.     

Effects of topical instillation of traditional herbal medicines,herbal extracts,and their components on prostaglandin E2-induced aqueous flare elevation in pigmented rabbits

PURPOSE: To evaluate the effect of topical instillation of traditional herbal medicines, herbal extracts, and their components on the elevation of aqueous flare induced by prostaglandin E(2) (PGE(2)) in pigmented rabbits. METHODS: Transcorneal diffusion of 25 micro g/mL of PGE(2) was carried out through a glass cylinder placed on the cornea to induce aqueous flare elevation in pigmented rabbits. Traditional herbal medicines, herbal extracts, and their components were topically instilled before the PGE(2) application. Aqueous flare was measured with a laser flare-cell meter. RESULTS: Two instillations, 60 and 30 minutes before PGE(2), of Kakkon-to, Sairei-to, Orengedoku-to, Senkanmeimoku-to, Scutellariae radix extract, Coptidis rhizoma extract, Gardeniae fructus extract, Phellodendri cortex extract, baicalein, baicalin, wogonin, crocetin, berberine, or glycyrrhizine did not inhibit the elevation induced by PGE(2). Two instillations, 60 and 30 minutes before PGE(2), of a Ligusticum wallichii extract (100 mg/mL) inhibited the elevation by 20%. Two instillations (5 and 3 hours before PGE(2)) of baicalein (1 mg/mL) or baicalin (5 mg/mL) inhibited the elevation by 16% and 24%, respectively. Two instillations, 5 and 3 hours before PGE(2), of wogonin, crocetin, berberine, or glycyrrhizine did not inhibit the elevation. CONCLUSION: Two instillations of Ligusticum wallichii extract 60 and 30 minutes before the PGE(2), and two instillations of baicalein or baicalin, 5 and 3 hours before the PGE(2), inhibited the PGE(2)-induced aqueous flare elevation in pigmented rabbits.     

Effects of tetramethylpyrazine on prostaglandin E(2)- and prostaglandin E(2) receptor agonist-induced disruption of blood-aqueous barrier in pigmented rabbits

PURPOSE: To evaluate the effect of tetramethylpyrazine on the elevation of aqueous flare and intraocular pressure (IOP) induced by prostaglandin (PG) E(2) and PGE(2) receptor (EP) agonists. METHODS: PGE(2) or EP agonists (11-deoxy PGE(1), EP(2) agonist; 17-phenyl trinor PGE(2), EP(1) and EP(3) agonist; or sulprostone, EP(1) and EP(3) agonist), 25 microg/mL, were transcorneally administered to pigmented rabbits. Animals were pretreated with tetramethylpyrazine intravenously (10 or 30 mg/kg) or topically (0.1% solution). Aqueous flare was measured using a laser flare-cell meter, and the intensity was expressed as the area under the curve (AUC). Intraocular pressure was measured using a noncontact tonometer. RESULTS: After administration of PGE(2), aqueous flare and IOP increased and then gradually decreased. The AUC of eyes pretreated with tetramethylpyrazine, 10 or 30 mg/kg, intravenously, or topical 0.1% solution, was significantly smaller than that of the controls. The mean Delta IOP of eyes pretreated with tetramethylpyrazine, 30 mg/kg intravenously, was significantly lower than that of the controls. After administration of 11-deoxy PGE(1), aqueous flare increased and then gradually decreased. 17-phenyl trinor PGE(2) and sulprostone did not disrupt the blood-aqueous barrier. The AUC of eyes pretreated with tetramethylpyrazine, 10 or 30 mg/kg, intravenously, before 11-deoxy PGE(1) application was significantly smaller than that of the controls. CONCLUSION: The results indicated that tetramethylpyrazine inhibited PGE(2)- or 11-deoxy PGE(1)-induced elevation of aqueous flare and IOP.     

Changes in aqueous flare and cells after mydriasis

The influence of a commonly used short-acting mydriatic agent, tropicamide-phenylephrine, on aqueous flare intensity and cell number was studied both in postsurgical cases and normal subjects. Measurements with a laser flare-cell meter were carried out in 40 patients who had undergone planned extracapsular cataract extraction with posterior chamber intraocular lens implantation. On the second postoperative day, 20 patients received one drop of a combined solution of 0.5% tropicamide and 0.5% phenylephrine, and the remaining patients received no mydriatic agents. Flare-cell meter measurements in the non-mydriasis group were rather difficult, and measurements in 12 out of 20 (60%) cases were discontinued. In the mydriasis group, flare intensity became significantly lower 2 hours after the application (P less than 0.01) and continued to decrease throughout the rest of the measurement period. The cell counts tended to decrease throughout the period after mydriasis and showed significantly lower values compared to the initial value (P less than 0.01). It was considered that measurements with this instrument in postoperative cases are best performed between 30 minutes to 1 hour after the application of the short-acting mydriatic agents. In normal human eyes, the effects of 0.5% phenylephrine-0.5% tropicamide, 0.4% tropicamide, and 5% phenylephrine on aqueous flare and cells were tested separately. Aqueous flare intensity was significantly decreased by tropicamide-phenylephrine at 1, 1.5 and 2 hours (P less than 0.05), by tropicamide at 1 and 1.5 hours (P less than 0.01), and by phenylephrine at 3 hours (P less than 0.01) after the application, respectively. Values returned to normal following these transient decreases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Tyndallometry of the anterior chamber with the Kowa FC-100 Laser FLare-Cell Meter

The laser flare-cell meter measures the scattered light intensity of a He-Ne laser in the aqueous of the anterior chamber. It allows a reliable quantitative determination of the flare and the number of cells in the aqueous humor. The aqueous flare intensities are significantly decreased by short-acting mydriatic agents such as 0.5% tropicamide and phenylephrine. Diurnal variations and an increase of the aqueous flare with increasing age were demonstrated.     

Effects of nilvadipine, nicardipine and verapamil on acute rise of aqueous flare induced by iris photocoagulation or intravenous lipopolysaccharides in pigmented rabbits

The effects of nilvadipine, nicardipine and verapamil on the acute rise of aqueous flare induced by argon laser photocoagulation of the iris or by intravenous injection of lipopolysaccharides (LPS, 0.5 microg/kg) were investigated in pigmented rabbits. Nilvadipine, nicardipine and verapamil were injected intravenously. Aqueous flare was measured with a laser flare cell meter. Following photocoagulation, aqueous flare increased, reached its maximum at 45-75 min and then decreased. After administration of LPS, aqueous flare increased, reached its maximum at 4 h and then returned to baseline levels at about 24 h. Flare reactions were inhibited by nilvadipine in a dose-dependent manner. The elevations were maximally inhibited by nilvadipine 30 min before photocoagulation or intravenous LPS. Two hundred micrograms per kilogram of nilvadipine inhibited 81% of photocoagulation-induced flare elevation, while the same dose of nicardipine and verapamil inhibited 19 and 9% of the elevation, respectively. The same dose of nilvadipine inhibited 51% of LPS-induced flare elevation, while the same dose of nicardipine and verapamil inhibited 6 and 4% of the elevation, respectively. In conclusion, nilvadipine inhibited the experimental elevation of aqueous flare more effectively than did nicardipine and verapamil.     

Effects of alpha(2)-adrenergic agonists on lipopolysaccharide-induced aqueous flare elevation in pigmented rabbits

PURPOSE: To evaluate the effects of the alpha(2)-adrenergic agonists (clonidine, apraclonidine, and guanfacine) on lipopolysaccharide (LPS)-induced aqueous flare elevation in pigmented rabbits. METHODS: Anterior uveitis was induced with an intravenous injection of LPS (0.5 microg/kg) in an ear vein. The reproducibility of experimental uveitis induced by LPS (0.5 microg/kg) was also determined. Clonidine (0.01, 0.05, 0.25, or 1%), apraclonidine (1%), or guanfacine (1%) was topically instilled in the right eye 30 and 5 minutes before and 30 minutes after LPS application (N = 6 animals, respectively). Clonidine (0.25%) was topically administered three times at 30-minute intervals from 240 or 120 minutes before, or 120 or 240 minutes after LPS application (N = 6 animals, respectively). Then 1 mg/kg of yohimbine was injected into an ear vein 30 minutes before each topical three-time instillation of clonidine 1%, apraclonidine 1% or guanfacine 1% (N = 6 animals, respectively). Aqueous flare was measured with a laser flare-cell meter. Aqueous flare elevation was expressed as the area under the curve (AUC) in arbitrary units. Rabbits received the first LPS intravenous injection, and the control values of the AUC were obtained. Three months later, the alpha(2)-agonist and the second LPS administration were given to the same animals. RESULTS: The AUCs (5,184 +/- 1,255 units) after the first application of LPS were similar to those (5,033 +/- 1,290) after the second application 3 months after the first administration. Topical instillation of clonidine inhibited LPS-induced aqueous flare elevation in a dose-dependent manner (0.01-0.25%). Topical instillation of clonidine 1%, apraclonidine 1% or guanfacine 1% inhibited LPS-induced aqueous flare elevation by 98 +/- 2.0% (mean +/- SD), 86 +/- 14% and 94 +/- 5.7%, respectively. Pretreatment with intravenous yohimbine prevented the inhibitory effect on flare elevation induced by each agent. CONCLUSION: The present findings suggested that topical instillation of some alpha(2)-agonists may have an inhibitory effect on ocular inflammation, which is mediated in part by alpha(2)-receptors.     

Randomized clinical trial of the efficacy and safety of tropicamide and phenylephrine in preoperative mydriasis for phacoemulsification

Purpose: To compare the mydriatic effect and safety between different concentrations of tropicamide and phenyle­phrine in preoperative mydriasis for phaco­emulsification. Methods: Two hundred and seventeen consecutive eyes in the same number of Chinese patients undergoing phaco­emulsification under local or topical anaesthesia in a university‐based eye hospital were analyzed. Patients were randomized into two groups by cluster randomization, each group receiving a different preoperative mydriatic regimen. Regimen A consisted of tropicamide 1.0% with phenylephrine 2.5%, and Regimen B consisted of tropicamide 0.5% with phenylephrine 0.5%. The main outcome measures were horizontal pupillary diameter, systolic, diastolic and pulse pressure and pulse rate. Results: The group who received Regimen A attained a mean horizontal pupillary diameter of 7.00 ± 1.06 mm. Their pupils were significantly larger than those receiving Regimen B (6.61 ± 1.03 mm, P = 0.007). No untoward cardiovascular effects were noted in either groups. Conclusion: Regimen A attained better preoperative mydriasis for phacoemulsification than Regimen B. Both regimens were safe with regard to their cardiovascular effects. The combination of tropicamide 1.0% and phenylephrine 2.5% is recommended as preoperative mydriatic for phacoemulsification in Chinese patients who have darkly pigmented irides.     

Influence of thymoxamine eye-drops on the mydriatic effect of tropicamide and phenylephrine alone and in combination

In a preliminary experiment in 12 healthy volunteers, one drop of thymoxamine 0.5% instilled into the conjunctival sac completely reversed the mydriasis produced by phenylephrine 2.5%, 5% and 10% after 20 minutes. In a second study in eight volunteers, thymoxamine 0.5% completely prevented the mydriasis produced by phenylephrine 2.5% and produced a miosis. It also completely reversed the mydriasis produced by tropicamide 0.5%. The mydriatic effect of tropicamide 0.5% plus phenylephrine 2.5%, however, was not completely reversed by thymoxamine 0.5% over a period of 180 minutes. Phenylephrine, tropicamide and thymoxamine are freely available for use by registered optometrists.     

Comparative study on the safety and efficacy of different cycloplegic agents in children with darkly pigmented irides

BACKGROUND: The ideal cycloplegic drug that is safe, effective and convenient in children is not yet available. This study aimed to evaluate the safety and efficacy of three cycloplegic regimens in hyperopic children with pigmented irides. The responses to cycloplegia in different age groups and presence of strabismus were also compared. METHODS: Tropicamide 0.5% and phenylephrine 0.5% (regimen I), tropicamide 1.0% and cyclopentolate 1.0% (regimen II), and atropine 1.0% (regimen III) were evaluated in 25 children using a crossover study design. Cycloplegic refractions were assessed. RESULTS: The mean age of the children was 5.7 +/- 2.0 years (range 2.5-10.8 years). Six (24.0%) of them had strabismus. The spherical equivalent (SE) refraction for regimens I, II and III were +5.11 +/- 2.04 D, +5.29 +/- 1.89 D and +5.71 +/- 1.90 D, respectively, and were significant different from the manifest SE (+3.95 +/- 2.17 D) (P < 0.001). There was no statistical difference between regimen I and II in children without strabismus (P = 0.258) or aged older than 5 years (P > 0.050). CONCLUSION: In older children, regimen I was as effective as regimen II and can be used to avoid cyclopentolate toxicity.     

Does prior instillation of a topical anesthetic enhance the effect of tropicamide?

Preinstillation of a topical anesthetic has been reported to increase the effect of subsequently applied mydriatics. We examined the effect of instilling 1 drop of proparacaine hydrochloride (0.5%) before applying 1 drop of tropicamide (1%). The results show that preanesthesia prolongs the mydriatic and the cycloplegic effects of tropicamide in eyes with either lightly or more heavily pigmented irides.