Interaction of adrenergic agents with alpha-melanocyte-stimulating hormone and infrared irradiation of the iris in the rabbit eye.

Breakdown of the blood aqueous barrier in the rabbit eye induces a protein leakage into the aqueous humor, seen as a flare in the anterior chamber. A barrier damage was induced by topical prostaglandin E2(PGE2), infrared irradiation of the iris, or alpha-melanocyte-stimulating hormone (alpha-MSH) given subcutaneously. The aqueous flare was measured quantitatively by means of a photoelectric instrument. The interference of adrenergic antagonists and agonists on the breakdown of the barrier was tested. The alpha-adrenergic antagonist phentolamine and the beta-adrenergic antagonist propranolol, given intravenously, had no effect on exogenously administered PGE2, but both antagonists reduced the flare response to infrared irradiation which is supposed to exert its effect via endogenous prostaglandin release. The alpha-MSH response was unaffected by phentolamine, whereas propranolol abolished the flare response to alpha-MSH totally. The PGE1 response was unaffected both by the alpha-adrenergic agonist noradrenaline and the beta-adrenergic agonist terbutalin sulfate, administered topically. Noradrenaline, however, inhibited the flare response to infrared irradiation and facilitated the flare response to alpha-MSH. Terbutalin sulfate worked synergistically with both infrared irradiation and alpha-MSH. It is assumed that alpha-MSH exerts its effect on the barrier via enhanced beta-adrenergic activity, whereas the effects caused by infrared irradiation seem conditioned by intact alpha- as well as beta-adrnergic receptor sites.     

The effect of timolol maleate on the disruption of the blood-aqueous barrier in the rabbit eye

A disruption of the blood-aqueous barrier in rabbit eyes was elicited by use of topical prostaglandin E2(PGE2), infrared irradiation of the iris, or by subcutaneous alpha-melanocyte-stimulating hormone (alpha-MSH). The aqueous flare provoked was measured quantitatively with a photoelectric instrument. The effect of the (topical) beta-adrenergic antagonist timolol maleate on the breakdown of the blood-aqueous barrier was tested. Timolol applied topically in very large doses had no effect on exogenously administered PGE2. However, even in a very small concentration applied topically, timolol reduced the flare response to both infrared irradiation and alpha-MSH. These results support the theory that the effect of alpha-MSH and infrared irradiation on the blood-aqueous barrier is dependent on intact beta-adrenergic receptor sites.     

The effect of polyphloretin phosphate on the aqueous flare response to alpha-melanocyte stimulating hormone

The breakdown of the blood aqueous barrier caused by topical prostaglandin E1 (PGE1), prostaglandin E2 (PGE2) or subcutaneous alpha-melanocyte stimulating hormone (alpha-MSH) was quantified by measurements of the aqueous flare seen in the anterior chamber. Polyphloretin phosphate (PPP) administration subcutaneously was found to effectively block the protein leakage caused by all three traumatic stimuli. The same dose of PPP given intravenously inhibited effectively the flare response to PGE1 and alpha-MSH, whereas the effect of PGE2 was only slightly decreased. Significant inhibition by subconjunctival PPP was not achieved for any of the three stimuli. Assuming that PPP is a specific PG-antagonist the present results support the eariler suggestion that PGs take part in the barrier damaging action of alpha-MSH. However, it cannot be excluded that PPP acts on a step subsequent to PG. This step might be common to PGs- and alpha-MSH-effects on the barrier, explaining why PPP inhibits both types of trauma.     

The effect of experimental uveitis on the uptake of prostaglandin E1 in the rabbit iris-ciliary body

Disruption of the blood-aqueous barrier in rabbits was elicited by infrared irradiation of the iris or by alpha-melanocyte stimulating hormone (alpha-MSH) given subcutaneously. One group of animals was pretreated with topical imidazole before the injection of alpha-MSH. The aqueous flare response was followed and the rabbits were killed at the expected height of the uveitis. The uptake of 3H-prostaglandin E1 in the iris with the ciliary body was then determined and found to be significantly decreased in the rabbits in which alpha-MSH had caused a severe damage of the blood-aqueous barrier. When alpha-MSH caused a more moderate aqueous flare response the prostaglandin uptake was on the contrary significantly increased. Pretreatment of the animals with topical imidazole enhanced parallelly the prostaglandin uptake and the aqueous flare response to alpha-MSH. Topical imidazole per se was found to increase the accumulation of prostaglandin. The prostaglandin uptake values were, however, unchanged in eyes in which infrared irradiation of the iris induced a moderate flare response.     

The effect of theophylline on the breakdown of the blood-aqueous barrier in the rabbit eye.

A disruption of the blood-aqueous barrier in rabbit eyes was elicited by topical prostaglandin E2, infrared irradiation of the iris, or subcutaneous alpha-melanocyte stimulating hormone (alpha-MSH). The course of the inflammatory reaction was followed by photoelectrical measurements of the aqueous flare in the anterior chamber. Pretreatment with intravenous theophylline, a phosphodiesterase inhibitor, significantly increased the protein leakage caused by prostaglandin E2 and alpha-MSH, but the response to infrared irradiation was slightly but not significantly enhanced. Intravenous theophylline given in higher doses caused per se an aqueous flare increase, which could not be inhibited by pretreatment with topical indomethacin. Our results indirectly indicate that accumulation of intraocular cAMP promotes a barrier damage and that cAMP might be the common effector of the barrier breakdown caused by prostaglandin as well as by nonprostaglandin agents.     

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.     

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.     

Inhibitory effect of nilvadipine on disruption of blood-aqueous barrier induced by prostaglandin E2 application in pigmented rabbits: A morphologic study

The purpose of the present study is to investigate the morphologic sites of breakdown in eyes pretreated with nilvadipine (a calcium channel blocker) that has been shown to inhibit the acute rise of aqueous flare induced by prostaglandin E2 (PGE2). Nilvadipine (100 microg/kg body weight) was injected intravenously in pigmented rabbits. Thirty minutes later, vehicle or PGE2 (10, 50 or 250 microg/ml) was applied on the cornea by use of a glass cylinder. Forty-five minutes later, the animals received horseradish peroxidase (HRP) intravenously and the eyes were enucleated. Distribution of HRP in the anterior segments was observed by electron microscopy. Without nilvadipine pretreatment, HRP was seen in the intercellular space of nonpigmented cells of the eyes treated with 50 microg/ml PGE2 and in the iris stroma of the eyes treated with 250 microg/ml PGE2. With nilvadipine pretreatment, HRP was not observed in these sites. Our results indicate that nilvadipine suppresses disruption of the different sites of the blood-aqueous barrier.     

Clinical evaluation of isopropyl unoprostone (Rescula), in the adjunctive treatment of primary open angle glaucoma

AIM: To investigate the clinical characteristics of docosanoid derivative, isopropyl unoprostone in the treatment of primary open angle glaucoma (POAG). MATERIAL AND METHODS: In 17 patients (22 eyes) with POAG we analysed prospectively the effect of Rescula upon intraocular pressure, aqueous flare, pupil size, ocular signs and symptoms. Patients were followed up every 2 weeks for at least 8 weeks with complete ocular examination. Concomitant topical therapeutics were used in the study: 0.5% Timolol--group I (16 eyes), and 0.5% Timolol + 2% Dorzolamide--group II (6 eyes). RESULTS: Mean (+/- SD) pretreatment pressure was 24.7 +/- 4.3 mm Hg in group I and it was reduced by 3.7 mm Hg (13.5%) (p < 0.05) at the end of the follow up. In group I Rescula was very effective (delta T% > 25%) in 6/16 eyes (37.5%) and it was ineffective (delta T% < 10%) in the same number of eyes. In group II pretreatment pressure was 24.8 +/- 2.6 mm Hg and it was reduced by 2.6 mm Hg (10.6%) (p = 0.1). Rescula induced no elevation of the aqueous flare during the treatment. No effect on pupil size was observed, either. Eye stinging/conjunctival hyperaemia was noted in 2/17 patients and punctate epitheliopathy in 1 patient (5.9%) that caused discontinuation of drops. CONCLUSIONS: Unoprostone produced significant additive effect to Timolol. Thus, it may be a valuable option for adjunctive therapy. However, interindividual differences need to be considered, as in some patients the response was insignificant.     

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.     

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.     

Mechanism of steroid action in ocular inflammation: Inhibition of prostaglandin production.

Prostaglandin E (PGE) concentration the aqueous humor of an intact rabbit eye was less than 0.1 ng. per milliliter and increased to 19 +/- 3 ng. per milliliter 60 minutes following paracentesis. The rise in PGE level was associated with clinical signs of ocular inflammation. Pretreatment with triamcinolone reduced both the accumulation of PGE in the aqueous humor and the inflammatory response following paracentesis. intravitreal injection of E. coli endotoxin into rabbit eyes increases PGE level in the anterior chamber to 72 +/- 17 ng. per milliliter and induced acute uveitis. slices of iris and ciliary body (ICB) derived from either rabbit eyes with endotoxin-induced uveitis or normal eyes were incubated for 60 to 240 minutes and the rate of PGE release into the medium was measured by radioimmunoassay. after a 4 hour incubation, the PGE release from inflamed ICB was threefold higher than that of normal ICB. incubation of inflamed ICB with hydrocortisone, or Millicorten (100 mug per milliliter) for 4 hours reduced PGE accumulation in the medium by 50 and 81 per cent, respectively. Aldosterone had no effect on the rate of PGE release from inflamed ICB throughout the incubation period. Hydrocortisone or Millicorten also reduced PGE tissue content of inflamed ICB by about 74 per cent during the period of incubation. Indomethacin (100 mug per milliliter) abolished PGE accumulation. The suppressive action of hydrocortisone on PGE release into the incubation medium was prevented by the addition of arachidonic acid (2 mug per milliliter), a substrate for prostaglandin synthesis. By contrast , the inhibitory action of indomethacin was not affected by provision of arachidonic acid. We suggest that glucocorticosteroids reduce PGE accumulation by limiting the availability of the substrate for prostaglandin biosynthesis and thus suppress the inflammatory response.     

The insensitivity of the chicken eye to the inflammatory effects of x-rays in contrast to its sensitivity to other inflammatory agents.

The effects of x-rays and three chemical agents, known to cause intraocular inflammation in mammalian eyes, were studied on the chicken eye because this species was reported to be insensitive to the cataractogenic effects of x-rays. Intravitreal injection of Shigella endotoxin and topical and/or intravitreal administration of PGE2, PGF2alpha, or arachidonic acid caused a breakdown of the blood-aqueous barrier, as indicated by flare and increased protein concentration in the aqueous humor. Following endotoxin injection, there was also a large accumulation of cells in the anterior chamber. The ocular inflammatory effects of endotoxin and arachidonic acid were inhibited by indomethacin. Thus the chicken eye reacts to these inflammatory agents in a manner similar to that previously described for the rabbit. In contrast, the inflammatory response which was reported to occur in the rabbit eye 3 to 4 hr after exposure to 500 or 1000 rads of x-rays was not observed in the chicken eye even after expsoure to 10,000 rads. Minimal flare and a small cellular infiltration were observed in some eyes only after extensive swelling of the surrounding tissues had developed. It is concluded that the insensitivity of the chicken eye to x-rays is due to some unique difference in the chain of events which mediates, or prevents, the effects of ionizing radiation rather than to a general insensivity to inflammatory agents.     

Phacoemulsification in Indian eyes with pseudoexfoliation syndrome.

PURPOSE: To evaluate the intraoperative and postoperative behavior after phacoemulsification in Indian eyes with pseudoexfoliation syndrome. SETTING: Iladevi Cataract & Intraocular Lens Research Centre, Ahmedabad, India. METHOD: Ninety eyes were prospectively evaluated. Group 1 (cohort) comprised 45 consecutive eyes with pseudoexfoliation and coexisting cataract and Group 2 (control), 45 consecutive normal eyes with senile cataract only. Phacoemulsification was performed by a single surgeon using a step-by-step, chop in situ, and lateral separation technique. An AcrySof intraocular lens was implanted in the bag in all eyes. Intraoperative observations included pupil size after maximal mydriasis, phakodonesis, zonular dehiscence, grade of cataract, and capsule tear/rupture. Postoperatively, intraocular pressure (IOP), best corrected visual acuity, aqueous flare/cell response, and the presence of posterior synechias were evaluated at 1 day and 1 month. A chi-square test was used for statistical analyses. RESULTS: The mean pupil size was significantly smaller in Group 1 (P =.0000). No eye in either group had phakodonesis. Sixty percent of eyes in Group 1 and 31% in Group 2 had a hard cataract (P =.008). Endocapsular phacoemulsification was performed in 82% of eyes in Group 1 and 84% of eyes in Group 2. Intraoperative complications such as zonular or capsular dehiscence were not seen in any eye. Postoperatively, IOP and aqueous cell response were comparable between groups (P =.11 and P = 0.81, respectively). A significantly higher flare response was observed in Group 1 (P =.000). The visual outcome at 1 month was similar between groups. CONCLUSIONS: The intraoperative performance of Indian eyes with pseudoexfoliation was comparable to that in normal eyes. A good surgical outcome is ensured by using an appropriate surgical technique. Apart from a higher flare response, the postoperative outcomes in eyes with pseudoexfoliation were within normal limits, and the outcome at 1 month was satisfactory.     

Changes in anterior chamber flare and cells following cataract surgery.

The laser flare cell meter allows rapid non-invasive quantification of aqueous flare and cells. In this prospective study laser photometry was used to document the recovery of the blood-aqueous barrier in 27 normal eyes following cataract surgery. Aqueous flare and cells were highest on the first postoperative day, declining rapidly in the first week and returning to preoperative levels by 3 months. In six eyes (22.2%) there was an increase in either flare and cells or flare alone during the first postoperative week which was associated with a delayed recovery of the blood-aqueous barrier for up to 1 month following surgery. A consensual flare response was found to occur in the fellow eye in five patients (18.5%).     

Experimental cataract models produced by repeated blunt mechanical stimulation and elucidation of the pathogenetic mechanism

PURPOSE: The pathogenesis of cataract produced by mechanical stimulation of the eye was studied using experimental models. METHODS: The eyes of rabbits (in vivo) and the extracted lenses of rats (in vitro) were subjected to vibration from an electric massage machine and tapping. The histological changes, aqueous flare score, protein and prostaglandin (PG) E2 levels in aqueous humor, and the rate of vitreous liquefaction were measured, and the involvement of apoptosis was examined in the rabbit model. RESULTS: In both models, mechanical stimulation resulted in a high frequency of opacification of the lens in the anterior or posterior subcapsular region. In the in vivo model, histopathological examination revealed vacuolar changes in the lens epithelium and swelling of lens fibers. Increases in aqueous flare score, protein level, PGE2 level, and the rate of vitreous liquefaction were confirmed. The involvement of apoptosis was not proven. CONCLUSION: Repeated mechanical stimulation of the eye produced lens opacification. In patients with atopic dermatitis, mechanical stimulation such as a habit of eye tapping may be the cause of or a factor in promoting cataract development.     

Inhibition of endotoxin-induced uveitis and potentiation of cyclooxygenase-2 protein expression by alpha-melanocyte-stimulating hormone

PURPOSE: The efficacy of alpha-melanocyte-stimulating hormone (alpha-MSH) on endotoxin-induced uveitis (EIU) was investigated in rats. Several studies have demonstrated that there are various inflammatory reactions mediated by an alpha-MSH receptor in macrophages. In addition, as it is known that cyclooxygenase (COX)-2 is induced by a variety of stimuli and plays an important role in inflammation, COX-2 expression was also investigated in macrophage cells treated with alpha-MSH in vitro to clarify its anti-inflammatory effect. METHODS: EIU was induced in male Lewis rats by a footpad injection of lipopolysaccharide (LPS). The number of infiltrating cells and protein concentration in the aqueous humor collected 24 hours after the LPS treatment was determined. The levels of prostaglandin (PG)-E2, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1 production were determined. RAW 264.7 cells were pretreated with various concentrations of alpha-MSH for 24 hours and subsequently incubated with 10 microg/mL LPS for 24 hours. COX-2 protein expression was analyzed by Western blot analysis. RESULTS: alpha-MSH suppressed the development of EIU in a dose-dependent fashion. The treatment with alpha-MSH reduced the PGE2, TNF-alpha, IL-6, and MCP-1 concentrations in aqueous humor. The COX-2 protein expression in the alpha-MSH group decreased. CONCLUSIONS: This study suggests that alpha-MSH has an antiocular inflammatory effect, by suppression of PGE2, TNF-alpha, IL-6, and MCP-1 production and blocking of COX-2 expression.     

Multiple dosing of prostaglandin F2 alpha or epinephrine on cynomolgus monkey eyes. II. Slit-lamp biomicroscopy, aqueous humor analysis, and fluorescein angiography

Prostaglandin (PG) F2 alpha (250 micrograms in 50 microliters saline) or epinephrine 2% solution (50 microliters) was topically applied twice daily for 2 weeks to one eye of six cynomolgus monkeys for each agent. Contralateral control eyes received their respective vehicles. A trace aqueous humor flare response occurred in some PGF2 alpha-treated eyes, which reached significance (P less than 0.05) only when observed 4 hr after the first or seventh dose. No significant anterior chamber cellular response was observed in treated as compared to control eyes. Slit-lamp biomicroscopic evaluation of the cornea, iris, and lens showed no differences in treated as compared to control eyes throughout the study. Aqueous humor samples were obtained from all eyes 4 hr after the ninth consecutive dose. Soluble protein concentration was significantly (P less than 0.01) greater in the PGF2 alpha-treated eyes (1.22 +/- 0.30 mg/ml) as compared to control (0.56 +/- 0.17 mg/ml) or to epinephrine-treated eyes (0.59 +/- 0.18 mg/ml). Microscopic examination of sediments obtained after centrifugation of the aqueous humor revealed no cells in experimental or control samples. Both PGF2 alpha and PGE2 levels were significantly (P less than 0.025) greater in PGF2 alpha-treated eyes, and showed a trend towards being greater in epinephrine-treated compared to control eyes. Neither cystoid macular edema nor other retinal abnormalities were evident by fluorescein angiography in any eyes during the second week of treatment. Multiple dosing of PGF2 alpha in monkey eyes does not appear to produce clinically significant adverse effects in either the anterior or posterior segment which would contraindicate its use in a multiple-dose clinical trial in glaucoma patients.     

Clinical application of laser flare-cell meter

Clinical application of the laser flare-cell meter was described. The instrument was developed for concurrent quantitative determinations of the flare and number of cells in the aqueous humor. Diurnal variations were demonstrated in the aqueous flare, and also an increase in the flare with increasing age. The effects of drugs on aqueous humor dynamics were also studied. Orally administered 500 mg of carbonic anhydrase inhibitor reduced the aqueous humor formation by one-third. Concurrent study with the laser flare-cell meter and slit-lamp microscopy in uveitis cases has revealed that the former instrument is superior to the latter in making a quantitative evaluation of inflammation in the anterior segment of the eye. A follow-up study of postoperative inflammation was performed in patients undergoing extracapsular cataract extraction with posterior chamber intraocular lens implantation. Cases with uneventful postoperative course showed intense flare on the first postoperative day followed by a rapid decrease. Cases with inflammation and fibrin had high aqueous flare which showed an increase even before detection of fibrin in the aqueous by slit-lamp microscopy. Topical 0.5% indomethacin treatment was shown to be effective in suppressing the postoperative increase in aqueous flare but had little effect on cell count. In cases undergoing Argon laser trabeculoplasty, the aqueous flare in the treated eyes was determined to be significantly higher than that in the fellow eyes for four weeks postoperatively (P less than 0.05). The laser flare-cell meter has made it possible to determine the flare and number of cells in the aqueous humor quantitatively. This capability differentiates the instrument from the slit-lamp microscope as well as the instruments previously developed for similar purposes. The laser flare-cell meter is a newly developed useful tool to investigate the pathophysiology of the eye.     

Aqueous flare elevation in the fellow eye after vitrectomy

OBJECTIVE: 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. PATIENTS AND METHODS: 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. RESULTS: 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). CONCLUSION: This study demonstrated that subclinical sympathetic reaction did occur in the fellow eyes after vitrectomy.