Aqueous Flare Elevation Research Articles

Aqueous Flare and Progression of Visual Field Loss in Patients With Retinitis Pigmentosa.

PurposeTo investigate the association between aqueous flare and progression of visual field loss using the Humphrey Field Analyzer in patients with retinitis pigmentosa (RP).MethodsWe examined a total of 101 eyes of 101 patients who were diagnosed with typical RP. Sixty-one percent of the patients were female, and the mean age of the total group was 47.4 years. Aqueous flare, visual field (by an Humphrey Field Analyzer, the central 10-2 SITA-Standard program), and optical coherence tomography measurements were obtained for all patients. The slope, which was derived from serial values of mean deviation, macular sensitivity, or foveal sensitivity for each eye with univariate linear regression, was used for analysis.ResultsAqueous flare values were significantly correlated with the mean deviation slope (r = −0.20, P = 0.046), macular sensitivity slope (r = −0.28, P = 0.005) and foveal sensitivity slope (r = −0.20, P = 0.047). The values of the retinal sensitivity slope significantly decreased as the aqueous flare level increased (all P < 0.05). These associations remained unchanged after adjustment for age, sex, and posterior subcapsular cataract, and epiretinal membrane.ConclusionsElevation of aqueous flare is a risk factor for the decline of central visual function in RP. Aqueous flare may be a useful marker for disease progression in RP.

Effects of topical adrenergic agents on prostaglandin E2-induced aqueous flare and intraocular pressure elevation in pigmented rabbits.

To evaluate the effects of signals through adrenergic receptors on the changes in the aqueous flare and intraocular pressure (IOP) induced by topical prostaglandin E2 (PGE2) in pigmented rabbits. Adrenergic agents were applied topically to pigmented Dutch rabbits, and PGE2 was then applied to induce an increase in the aqueous flare and IOP. The degree of aqueous flare was measured with a laser flare meter, and the IOP was measured with a rebound tonometer. Measurements were made every 30 min after the PGE2 had been applied for 2 h and at 4.0 and 4.5 h. Repeated measure analysis of variance and Dunnett's post hoc tests were used for the statistical analyses. The topical application of PGE-2 increased the aqueous flare for more than 4.5 h. The topical instillation of 1.0 % apraclonidine significantly inhibited the increase in the PGE2-induced aqueous flare by 75.1 %, of 0.1 % brimonidine by 57.2 %, of 0.04 % dipivefrin by 57.4 %, and a combination of 0.1 % brimonidine and 5 % phenylephrine by 78.9 %. Topical 5.0 % phenylephrine and 0.05 % isoproterenol had little effect on the aqueous flare elevation induced by PGE2. The IOP increased 0.5 h after the topical application of PGE-2. Topical 1.0 % apraclonidine, 0.1 % brimonidine, 0.1 % dipivefrin, and the combination of 0.1 % brimonidine and 5.0 % phenylephrine significantly inhibited the PGE2-induced IOP elevation. However, topical 5.0 % phenylephrine and 0.05 % isoproterenol did not significantly inhibit the IOP elevation caused by PGE2. Signaling by the α2 receptor inhibits both the PGE2-induced flare and IOP elevation caused by topical PGE2 application.

The Effect of Hochu-ekki-to on Aqueous Flare Elevation after Small- Incision Cataract Surgery

Background: In Japan, Kampo medicines (Japanese herbal medicines) are often used as adjuvant therapy to Western medicines. In the present study, the effect of Kampo medicine Hochu-ekki-to (HOT) on aqueous flare elevation (AFE) after small-incision cataract surgery (SICS) was investigated. Materials and methods: Fifteen patients (24 eyes) with age-related cataracts that underwent SICS were prospectively studied. Patients with glaucoma, diabetes, or uveitis were excluded from the study. HOT was orally administered to seven subjects (12 eyes) from the day of surgery through postoperative week 4. Control group subjects (eight subjects; 12 eyes) did not receive HOT. Both groups received the same nonsteroidal, steroidal, and antibacterial eye drops before and after surgery. AFE was measured preoperatively and postoperatively. Results: AFE at postoperative weeks 2 and 4 was significantly lower in the HOT group than in the control group. Conclusion: These results suggest that HOT is effective in suppressing AFE.

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 µg/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 µmol/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 µmol/kg) and FR188582 (15 µmol/kg) 30 min before PGE₂ application inhibited 61 ± 8% of flare elevation. Dexamethasone phosphate disodium (15 µmol/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 Topical Instillation of Traditional Herbal Medicines, Herbal Extracts, and Their Components on Prostaglandin E 2-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 μg/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 oral administration of Gardeniae fructus extract and intravenous injection of crocetin on lipopolysaccharide- and prostaglandin E2-induced elevation of aqueous flare in pigmented rabbits.

The purpose of this study was to evaluate the effects of extracts of Coptidis rhizoma, Phellodendri cortex and Gardeniae fructus, which are medicinal herbs in Orengedoku-to (Huanglin-Jie-Du-Tang in Chinese), and crocetin (a major component of Gardeniae fructus) on experimental elevation of aqueous flare in pigmented rabbits. To produce aqueous flare elevation, 0.5 microg/kg lipopolysaccharide (LPS) was injected into the ear vein, or prostaglandin E2 (PGE2) 25 microg/ml, was applied to the cornea by means of a glass cylinder. Animals were pretreated by oral administration of 150 g/day of food containing 0.15% (w/w) extract powder of Coptidis rhizoma, 0.10% (w/w) extract powder of Phellodendri cortex or 0.15% (w/w) extract powder of Gardeniae fructus for 4 days, or by intravenous injection of crocetin, 0.3, 3, 30 or 300 microg/kg, 30 minutes before aqueous flare elevation. 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. The AUC of LPS- and PGE2-induced aqueous flare elevation was 4685 and 1386 arbitrary units, respectively. Pretreatment by oral administration of 0.15% (w/w) extract of Coptidis rhizoma or 0.10% (w/w) extract of Phellodendri cortex did not inhibit LPS-induced aqueous flare elevation. Pretreatment by oral administration of 0.15% extract of Gardeniae fructus suppressed LPS-induced aqueous flare elevation (AUC: 1411 arbitrary units). Pretreatment by intravenous injection of 3, 30 or 300 microg/kg of crocetin-inhibited LPS-induced aqueous flare elevation in a dose-dependent manner. Pretreatment with 3 or 30 microg/kg of crocetin did not inhibit PGE2-induced aqueous flare elevation, but 300 microg/kg of crocetin inhibited PGE2-induced aqueous flare elevation (AUC: 918 arbitrary units).

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 µg/ml (7.09 × 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 Topical Mydriatics and Vasoconstrictors on Prostaglandin-E2-Induced Aqueous Flare Elevation in Pigmented Rabbits

We evaluated the effects of topical instillation of mydriatics and vasoconstrictors on prostaglandin E₂ (PGE₂) induced aqueous flare elevation in pigmented rabbits. Transcorneal diffusion of PGE₂ (25 µg/ml) by means of a glass cylinder produced aqueous flare elevation. Mydriatics (atropine sulfate, tropicamide, tropicamide plus phenylephrine hydrochloride, phenylephrine hydrochloride, and cyclopentolate hydrochloride) or vasoconstrictors (naphazoline nitrate and tramazoline hydrochloride) were topically administered before PGE₂ application. Aqueous flare was measured with a laser flare-cell meter. One or two instillations of atropine sulfate 1.0%, tropicamide 0.4%, tropicamide 0.5% plus phenylephrine hydrochloride 0.5%, phenylephrine hydrochloride 5.0%, cyclopentrate hydrochloride 1.0%, and naphazoline nitrate 0.05% did not inhibit PGE₂-induced aqueous flare elevation. Tramazoline hydrochloride 0.118% inhibited significantly (p < 0.05) PGE₂-induced aqueous flare elevation. It is possible that vasoconstriction may be involved partly in inhibition of PGE₂-induced aqueous flare elevation by some drugs in pigmented rabbits.

Effect of Topical Iganidipine on Experimental Elevation of Aqueous Flare Induced by Prostaglandin E2 and EP Agonists in Pigmented Rabbits

We evaluated the role of topical iganidipine on experimental aqueous flare elevation in rabbits. Transcorneal diffusion of prostaglandin E₂ (PGE₂), 25 µg/ml or 7.09 × 10^–2 mmol/l, or highly selective agonists for prostaglandin E₂ receptor subtypes (EP), 25 µg/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 PGE₂ 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 PGE₂-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.

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 µg/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 Isopropyl Unoprostone, Latanoprost, and Prostaglandin E2 on Acute Rise of Aqueous Flare in Pigmented Rabbits

Purpose: To evaluate the effect of isopropyl unoprostone, latanoprost, and prostaglandin E₂ (PGE₂) on aqueous flare elevation. Methods: Isopropyl unoprostone (0.12%) or latanoprost (0.005%) was topically instilled. Transcorneal diffusion of PGE₂, 25 µg/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 PGE₂. Latanoprost did not induce flare elevation. Conclusion: Isopropyl unoprostone induced aqueous flare elevation in rabbits, and latanoprost did not produce aqueous flare elevation.

Effects of Orengedoku-to and Scutellariae radix extract on aqueous flare elevation induced by intravitreal IL-1alpha in pigmented rabbits.

We investigated the effects of Orengedoku-to (huanglian-jie-du-tang in Chinese) and Scutellariae radix extract on experimental aqueous flare elevation in pigmented rabbits. To produce the elevation of aqueous flare in rabbits, interleukin-1 alpha (IL-1alpha) was injected intravitreally. Animals were pretreated with oral administration of 150 g/day of food containing 0.07%, 0.2% or 0.7% (w/w) Orengedoku-to; or 0.02%, 0.07% or 0.2% Scutellariae radix extract for 5 days. The animals were further treated with the same food for 7 days after intravitreal injection of IL-1alpha. Aqueous flare was measured with a laser flare-cell meter. Treatment with 0.2% or 0.7% Orengedoku-to and 0.07% or 0.2% Scutellariae radix extract significantly (p < 0.05) suppressed elevation of aqueous flare induced by IL-1alpha. Thus, orengedoku-to and Scutellariae radix extract have an inhibitory effect on experimental elevation of aqueous flare induced by IL-1alpha in 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 μg/mL (7.09 × 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.

Aqueous flare elevation induced by transcorneal application of highly selective agonists for prostaglandin E2 receptor subtypes in pigmented rabbits: Effect of tetramethylpyrazine

We examined the disruptive effect of highly selective agonists for prostaglandin E 2 receptor subtypes (EP 1, EP 2, EP 3 and EP 4) on the blood-aqueous barrier, and evaluated the inhibitory effect of tetramethylpyrazine, an active component of Ligusticum wallichii, on the elevation of aqueous flare induced by the EP agonists in pigmented rabbits. Highly selective EP agonists (ONO-DI-004, EP 1 agonist; ONO-AE1-259-01, EP 2 agonist; ONO-AE-248, EP 3 agonist; ONO-AE1-329, EP 4 agonist) at 12.5 to 250 μg/ml were transcorneally administered to the eyes of pigmented rabbits using a glass cylinder. Animals were pretreated intravenously with tetramethylpyrazine (10 or 30 mg/kg) 30 minutes before application of the EP 2 or the EP 4 agonist. 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. After administration of ONO-AE1-259-01 or ONO-AE1-329, aqueous flare increased and then gradually decreased. ONO-DI-004 and ONO-AE-248 had almost no effect on aqueous flare elevation. The AUC of eyes in rabbits pretreated with tetramethylpyrazine, 10 or 30 mg/kg i.v., was significantly smaller than that of eyes in rabbits treated with ONO-AE1-259-01 alone. The AUC of eyes in rabbits pretreated with tetramethylpyrazine, 10 or 30 mg/kg i.v., was not significantly smaller than that of eyes in rabbits treated with ONO-AE1-329 only. The results indicated that EP 2 and EP 4 agonists induced aqueous flare elevation in pigmented rabbits, and that tetramethylpyrazine inhibited the aqueous flare elevation induced by the EP 2 agonist but did not suppress the elevation induced by the EP 4 agonist.

Effects of α2-Adrenergic Agonists on Lipopolysaccharide-induced Aqueous Flare Elevation in Pigmented Rabbits

Purpose: To evaluate the effects of the α 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 μg/kg) in an ear vein. The reproducibility of experimental uveitis induced by LPS (0.5 μg/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 α 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 α 2-agonists may have an inhibitory effect on ocular inflammation, which is mediated in part by α 2-receptors.

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 μg/mL, was applied to the cornea with the use of a glass cylinder, or lipopolysaccharides (LPS), 0.5 μg/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 μg/kg or 600 μg/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 μg/kg of baicalein, baicalin, or wogonin inhibited LPS-induced aqueous flare elevation (AUC: 2,289, 2,163, and 1,509, respectively). Pretreatment with 60 μg/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.

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 μg/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 Δ 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.

Ultrasound biomicroscopic analysis of posterior chamber intraocular lenses with transscleral sulcus suture

Objective To investigate the postoperative problems of intraocular lenses (IOLs) with transscleral sulcus suture. Design Retrospective observational case series. Participants Forty-one subjects (43 eyes) were included. Intervention All eyes had undergone transscleral sulcus suture of IOLs. Surgeries were all performed by surgeons in our clinic using the same technique. Main outcome measures Ultrasound biomicroscopy of the suture sites, their surrounding structures, and central anterior chamber depth. Other parameters studied included visual acuity, aqueous flare, and routine ophthalmic examinations. Results Thirty-two of 86 haptics were sutured at the ciliary sulcus (CS) region and 29 at the ciliary process region, which was the space between CS and pars plicata, and 25 posterior to pars plicata. We designated the cases with at least one haptic located in the CS region as the anterior group, and the other cases as the posterior group. In the anterior group, anterior chamber depth was significantly more shallow than in the fellow eye in which IOLs were fixed in the bag ( P = 0.049). There was a statistically greater incidence of IOL iris contact in the anterior group than in the posterior group ( P = 0.00057). Pigment dispersion was seen in seven cases, all of which were classified as anterior group. Eyes in the posterior group had more aqueous flare than their fellow eyes ( P = 0.014). Two cases, in which more than two lines of postoperative best-corrected visual acuity was lost because of macular degeneration after cystoid macular edema, showed marked elevation of aqueous flare in the sutured eyes compared with their fellow eyes. Forty-one of 86 haptics had vitreous incarceration. Conclusions This technique has many limitations: the difficulty of suturing precisely at the ciliary sulcus, IOL iris contact, pigment dispersion, high aqueous flare, and vitreous incarceration. These induce two major postoperative complications: chronic inflammation and influence on the adjacent vitreous such as vitreous incarceration. The suturing technique and instruments need to be improved to diminish such complications.

Aqueous Flare Elevation in the Fellow Eye After Vitrectomy

Aqueous flare elevation has been shown to occur in the fellow eye after cataract surgery. This study tests whether such subclinical sympathetic reaction also takes place after vitrectomy. In a prospective clinical study, preoperative and postoperative 2-week levels of aqueous flare in the fellow eyes of 38 patients who underwent vitrectomy during a 6-month period were measured with a laser flare-cell meter. Aqueous flare levels in the fellow eyes 2 weeks after vitrectomy (mean, 15.70 photon counts/millisecond) were significantly higher than preoperative flare levels (mean, 11.78 photon counts/millisecond, Wilcoxon's signed rank test, P = 0.04). This study demonstrated that subclinical sympathetic reaction did occur in the fellow eyes after vitrectomy.

Effects of Topical Clonidine on Prostaglandin-E2-Induced Aqueous Flare Elevation in Pigmented Rabbits

We evaluated the role of topical clonidine on experimental ocular inflammation. Transcorneal diffusion of prostaglandin (PG) E₂, 7.09 × 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 PGE₂-induced aqueous flare elevation. Instillation of clonidine at 60 or 30 min before and 10 min after PGE₂ 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 α₂-receptors.