Endotoxin-induced uveitis in the rat

Intraocular inflammation was induced in the rat by footpad injection of salmonella endotoxin in order to study the influence of chemical inflammation mediators in this uveitis model. Ocular inflammation was assessed 1, 6, 18, 24 and 72 h after endotoxin administration as well as in control rats, by measuring aqueous protein concentration, aqueous inflammatory cell content, and pupillary diameter. Thromboxane B2 (TXB2), prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2-alpha), leukotriene B4 (LTB4), and substance P were simultaneously measured in the aqueous humor by radioimmunoassay. Inflammation parameters peaked at 18 h. TXB2 was already significantly elevated at 1 h. PGE2 peak values of 2.7 ng/ml were reached at 18 h. PGF2-alpha was never significantly raised over control values. LTB4 peaked at 18 h, together with a polymorphonuclear peak. Substance P was significantly elevated after 6 h. It is concluded that maximal uveitis in this model occurs at 18 h. TXB2 is an early mediator, and PGE2 is probably implicated in blood-ocular barrier disruption for which levels as high as 2.7 ng/ml in aqueous seem necessary. PGF2-alpha does not play a major role in this model, while LTB4 seems to be the main chemotactic factor for polymorphonuclears (PMNs) in the anterior chamber and substance P is clearly related to pupil miosis.     

Synthesis of prostaglandin E in rabbit eyes with topically applied epinephrine

Using radioimmunoassay techniques, we measured the amounts of prostaglandin E (PGE) in the aqueous humor and vitreous body of 22 phakic and ten aphakic rabbit eyes. Either epinephrine and placebo, epinephrine and indomethacin, indomethacin and placebo, or placebo and placebo were administered topically for 5 months. Treatment of aphakic eyes was initiated 1 month after intracapsular lens extraction. Topically applied epinephrine apparently induced the synthesis of prostaglandin, manifested by elevated PGE in the aqueous and vitreous. Phakic eyes treated with epinephrine and placebo had mean PGE levels of 407.33 pg/ml in the aqueous and 177.0 pg/ml in the vitreous, whereas control eyes given only placebo had mean levels of 165.83 in aqueous and 59.17 in vitreous. Topically applied indomethacin inhibited epinephrine-induced synthesis of PGE in the aqueous humor, but had no significant effect in the vitreous. PGE levels, higher in placebo-treated aphakic eyes than in phakic ones, were elevated further by epinephrine treatment (from 388.40 to 1851.60 pg/ml in aqueous of aphakic eyes, and from 236.40 to 850.60 pg/ml in vitreous also of aphakic eyes). Our findings relate to the pathogenesis of epinephrine-induced maculopathy and to the mechanism of the ocular hypotensive effect of epinephrine.     

Efficacy of low concentrations of ketorolac tromethamine in animal models of ocular inflammation.

PURPOSE: To determine if topical ophthalmic application of ketorolac tromethamine concentrations below 0.5% can block the biochemical and physiological processes associated with chemically induced ocular inflammation in rabbits. METHODS: Ocular inflammation was induced in rabbits by intravenous (i.v.) injection of endotoxin (2.5 microg/kg) isolated from Salmonella typhimurium, or by a topical application of arachidonic acid (1.0%). The effect of ketorolac (at concentrations ranging from 0.001%-0.5%) on ocular inflammation was determined by measuring changes in the blood-aqueous barrier, using fluorophotometry (dextran-isothiocyanate-fluorescein; FITC-dextran 2%) and by measuring changes in aqueous humor protein concentrations. Changes in aqueous humor prostaglandin E(2) (PGE(2)) concentrations were also measured. RESULTS: Ketorolac 0.01%-0.5% produced substantial decreases in endotoxin-induced fluorescein leakage into the aqueous humor. The decrease produced by ketorolac 0.1% was comparable to that produced by ketorolac 0.5%. Ketorolac 0.1%-0.5% produced substantial decreases in endotoxin-induced increases in prostaglandin concentrations in the aqueous humor, and in arachidonic acid-induced protein leakage into the aqueous humor. CONCLUSIONS: Topical application of ketorolac concentrations as low as 0.01%-0.1% significantly reduce chemically induced ocular inflammation in rabbits.     

The effect of vasoactive intestinal polypeptide (VIP) on ocular inflammation in rabbit ocular tissue

Intravitreous injection of vasoactive intestinal polypeptide (VIP) induced ocular inflammation in albino rabbits. Protein amounts and cell numbers in aqueous humor were measured. The effect of VIP on the release of cyclic AMP (cAMP) and prostaglandin E2 (PGE2) from the isolated albino rabbit irides was investigated. Mydriatic response was obtained by intravitreous injection of 0.5 microgram or less VIP. 5 microgram or more of VIP induced miosis and breakdown of the blood aqueous barrier. Intravitreous injection of VIP induced on increase of cAMP in the aqueous humor dose-dependently and a slight increase of PGE2. VIP induced a dose-dependent increase of cAMP release and slightly inhibit PGE2 release from isolated irides. In this study, a large quantity of VIP was injected intravitreously induced breakdown of the blood aqueous barrier. The effect of VIP on isolated irides was to activate the release of cAMP and to inhibit that of PGE2.     

Aqueous humor in lens repair and cell proliferation

The intracameral infusion of 1% methylene blue solution produces a well-defined retropupillary lesion marked by the destruction of lenticular epithelium, fiber-cell damage and cataract-like opacification. When lenses are explanted to a maintenance medium 18 hr or more after chemical insult, a substantial proliferative response (DNA synthesis and mitosis) ensues. This hyperplastic response is comparable to that noted after dye-injury under entirely in situ conditions. However, if the lenses are explanted during the initial 12 hr subsequent to injury both DNA synthesis and mitosis fail to occur in more than 93% of cases. The mitotic response is restored if such injured lenses are cultured in the presence of aqueous humor isolated from dye-injured eyes. Moreover, such “injury aqueous humor”, which contains elevated levels of protein, induces a pronounced mitotic response in the epithelium of non-injured lenses maintained in organ culture. The traumatized eye, therefore, contains a mitogenic factor that is transferable through the aqueous humor. Ocular trauma or inflammation generally brings about an altered blood-aqueous barrier and it may be that this change in the lens environment is associated with the promotion of unscheduled rounds of cellular proliferation in otherwise normal lens epithelium.     

Effects of blue honeysuckle (Lonicera caerulea L.) extract on lipopolysaccharide-induced inflammation in vitro and in vivo

The aim of the present study was to investigate the effects of blue honeysuckle extract (BHE), which contains high level of phenolic compounds, on endotoxin-induced uveitis (EIU). Male Lewis rats were randomly divided into 5 groups with 14 rats in each (eight rats for collection of aqueous humor, six rats for histologic examination). EIU was induced by a footpad injection of lipopolysaccharide (LPS). 1, 10, or 100 mg of BHE was injected intravenously immediately after LPS injection. The aqueous humor was collected at 24 h after LPS injection, the number of infiltrating cells, protein concentration, nitric oxide (NO), tumor necrosis factor (TNF)-alpha, and prostaglandin (PG)-E2 levels in the aqueous humor were determined. Some eyes were enucleated for histologic examination and immunohistochemical analysis. Immunohistochemical staining with a monoclonal antibody against activated nuclear factor (NF)-kappaB was performed to evaluate the effect of BHE on NF-kappaB activation. To further clarify the anti-inflammatory effect, RAW264.7 cells (a mouse macrophage cell line) were stimulated with LPS in the presence or absence of BHE and its major phenolics, cyanidin 3-glucoside (C3G), cyanidin 3-rutinoside (C3R), chlorogenic acid (CA). Expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) were analyzed by Western blot method. BHE treatment significantly reduced the inflammatory cell infiltration, the protein concentration, the levels of NO, TNF-alpha and PGE2 in the aqueous humor and improved histologic status of the ocular tissue. The number of activated NF-kappaB-positive cells was lower in the iris-ciliary body treated with BHE at 3 h after LPS injection. BHE significantly suppressed the production of NO, PGE2 and TNF-alpha in the culture medium as well as the expression of iNOS and COX-2 by LPS-stimulated RAW264.7 cells in a dose-dependent fashion. C3G, C3R and CA showed no or weak inhibitory effects on the level of inflammatory mediators and the expression of iNOS and COX-2. These results suggest that BHE attenuates the degree of inflammation in eyes with EIU by inhibiting the NF-kappaB dependent signaling pathway and the subsequent production of proinflammatory mediators.     

Elevation of glucose in ocular compartments of developing chick embryos with glucocorticoid-induced cataract

When 15-day-old developing chick embryos were administered hydrocortisone hemisuccinate sodium (HC:0.25 mumol per egg) the concentration of glucose in both the aqueous humor and the vitreous body began to increase significantly after 3 hr and reached 24.4 +/- 0.3 mM and 22.3 +/- 0.9 mM, respectively, at 48 hr. Thereafter, the levels decreased to the control by 100 hr. During the treatment period, the glucose concentration of the control aqueous humor and vitreous body remained at approximately 7.5 mM and 4.3 mM, respectively. These changes in glucose after HC administration were quite different from that of the lens in regard to the extent of increase and the lag time required to produce glucose accumulation. By in vitro and in ovo experiments, it was found that the environment surrounding lens, medium and ocular fluids, greatly influenced the level of lenticular glucose rather than any changes metabolic activities in the lens. A glucose threshold of near 15 mM in milieu was required to promote the accumulation glucose in the lens.     

Induction of mitosis in ocular tissue by chemotoxic agents.

Ocular inflammation has been induced in a number of species by a variety of chemical agents, including methylene blue. Initial cell destruction and subsequent repopulation by mitogenesis in lens epithelium and corneal endothelium were observed using techniques for living and fixed tissue. During the course of the chemical inflammation response, the lens displayed a prominent, anterior pole subcapsular opacity underlying the area of maximal epithelial destruction. Near-normal transparency returned with recovery of the lens tissue cytoarchitecture. Elevated protein concentrations in aqueous humor were found throughout the course of the experiments. Similar alterations in aqueous humor were observed in the course of immunogenic uveitis although lenticular or corneal endothelial destruction and subsequent proliferation were not detected.     

Does the lens serve as a 'sink' for iron during ocular inflammation?

Twenty-four hours after induction of ocular inflammation by intravitreal injection of endotoxin (10 ng), the intraocular fluid (IOF, aqueous and vitreous humors) concentration of iron (Fe) increased. This was presumably due to entry of the plasma Fe-binding protein, transferrin, into the IOFs through disrupted blood ocular barriers. After 1 day of inflammation the Fe concentration in lenses from the inflamed eye was 60% greater than that measured in contralateral control lenses. By day 15, lens Fe concentration had returned to levels of the contralateral control lenses. There was a distinct relationship between the dose of endotoxin used and the amount of Fe accumulated by the lens. The Fe concentration in lenses from eyes injected with 100 ng endotoxin was 0.376 +/- 0.027 micrograms g-1 wet weight compared to 0.214 +/- 0.014 micrograms g-1 in lenses from eyes injected with 0.25 ng endotoxin. In a previous study, copper (Cu) concentration in the IOFs was elevated to the same extent as Fe in response to intravitreal injection of endotoxin. However, in the present study, lenticular Cu concentration was unaltered at the highest (100 ng) dose of endotoxin. Since the increase in lens uptake was selective for Fe, there may be a specific Fe uptake mechanism in this ocular tissue. The physiological reasons for and possible pathological consequences of such a process are discussed.     

Transient loss of prostaglandin synthetic capacity in rabbit iris-ciliary body following anterior chamber paracentesis

The trauma-induced acute ocular inflammatory response has been characterized by investigating the kinetics of blood-aqueous barrier (BAB) breakdown, prostaglandin (PG) accumulation in the aqueous humor, and cyclooxygenase (PGH synthase) activity of the iris-ciliary body (ICB) following paracentesis in the NZA rabbit. BAB breakdown was assessed by quantifying plasma protein extravasation into the anterior chamber. PGE 2 and 6-keto-PGF 1a concentrations in the aqueous humor were quantified by radioimmunoassay. The capacity of ICB tissue homogenates to generate eicosanoids from exogenously supplied [1- 14 C]-arachidonic acid was assessed radiometrically by HPLC. Paracentesis resulted in a rapid and dramatic increase in aqueous humor PGE 2 concentrations. Within 10 minutes, PGE 2 concentrations increased 937-fold, from 6.2±4.9 pg/ml to maximal concentrations of 5810±3829 pg/ml. PG synthesis was followed temporally by an increase in aqueous humor protein, with peak levels (53.1 mg/ml) achieved within 30 minutes post paracentesis. Both PGE 2 and protein levels gradually declined to near baseline levels 48 hours after trauma. ICB homogenates from naive animals produced significant amounts of eicosanoids (total PG=2.95 nmol/10 min/100 mg tissue). HHT (12 hydroxy-heptadecatrienoic acid) was produced in the greatest quantity, followed by PGE 2 , PGI 2 , and TXB 2 /PGF 2a. Notably, following paracentesis, eicosanoid synthesis by the isolated ICB was observed to diminish abruptly. Formation of all eicosanoids was uniformly reduced by ? 40% five minutes following paracentesis, with an 81% decrease in synthetic activity at 15 minutes. Eicosanoid synthetic capacity was only restored to baseline 48 hours post paracentesis. These findings suggest that, following ocular trauma, temporal changes occur in ICB PG synthetic activity that may impact on the selection of an optimal dosing paradigm for efficacy testing of topically administered NSAIDs.     

The effects of naringin and naringenin on endotoxin-induced uveitis in rats.

The aim of this study was to investigate the efficacy of naringin and naringenin on endotoxin- induced uveitis (EIU) in rats. EIU was induced in male Lewis rats by a footpad injection of lipopolysaccharide (LPS). The rats were injected intravenously with 0.4, 4, or 40 microg/kg naringin or naringenin. Each compound was administered three times, simultaneously, 30 min before and after the actual LPS injection. The aqueous humor was collected 24 h later from both eyes, and the number of cells infiltrating into the aqueous humor and the aqueous humor protein concentration were measured. The levels of prostaglandin E2 (PGE2) and nitric oxide (NO) were determined. Naringin and naringenin suppressed the development of EIU in a dose-dependent fashion. Both treatments with naringin and naringenin produced reductions in PGE2 and NO concentrations in the aqueous humor. In particular, 40 microM/kg of naringin and naringenin suppressed increases in cell count owing to LPS treatment by 31% and 38%, respectively. The possible mechanism for the antiocular inflammatory effect may be the suppression of PGE2 and NO by naringin and naringenin.     

Endotoxin-induced uveitis in rats: morphological and biochemical study

Inflammation induced by systemic injection of endotoxin can be a good model for endogenous uveitis since ocular inflammation is induced without manipulating the eye. We carried out morphological and biochemical studies in Lewis rats to evaluate the breakdown of the blood-ocular barrier following injection of endotoxin (1 mg/rat) in footpads. Vasodilation was observed as early as 3 hours and became maximum at 18-24 hours after the injection. Unlike in the eye, no inflammatory changes were observed in other organs. Protein and cell contents in the aqueous humor increased significantly as early as 3 hours after the injection and reached a peak level at 24 hours. The protein content returned to the normal level in the following several days, while cells in the aqueous humor remained at a high level even 1 week after the injection. The time-course of the pupillary size was very similar to that of the protein concentration. Furthermore, we examined leukotrienes (LTs) levels in aqueous humor by high-pressure liquid chromatography. LTD4 was detected in the aqueous humor at 6 hours and reached its peak level at 24 hours. The present data indicates that the systemic injection of endotoxin causes the disruption of the blood-ocular barrier soon after the injection and inflammation becomes maximum in 18-24 hours. This model can be used for studying endogenous uveitis and the disruption of the blood-ocular barrier without direct trauma to the eye.     

The lens influences aqueous humor levels of transforming growth factor-β2

Background: Transforming growth factor-beta 2 (TGF-β2) is a pluripotent cytokine which has been suggested to play a number of roles in ocular physiologic and pathologic states. Intraocular fluid (IOF) levels of TGF-β2 are quite high. Although the sources of ocular TGF-β are not completely defined, the retinal pigment epithelium, the epithelium of the ciliary body and trabecular meshwork cells all secrete it. In this study we utilized canine lens and rabbit ciliary pigmented epithelial cell cultures to quantitate the in vitro secretion of TGF-β2. In addition, the effects of aphakia or the presence of cataractous lenses on IOF TGF-β2 levels were determined. · Methods: Lens and ciliary body epithelial cell culture supernatants and aqueous humors were assayed for total TGF-β2 levels by ELISA and bioassay. · Results: TGF-β2 accumulated in the media bathing lens epithelial cell cultures (0.7 ± 0.03 ng/ml at day 2) and ciliary pigmented epithelial cell cultures (0.8 ± 0.06 ng/ml at day 2) in a time-dependent manner. Surprisingly, aqueous humor from aphakic rabbit eyes contained significantly higher levels of TGF-β2 than their contralateral phakic controls. Furthermore, aqueous humor from canine eyes with cataracts also contained significantly higher levels of TGF-β2 than normal eyes. · Conclusions: These results suggest that the lens secretes TGF-β2 and that the presence and status of the lens may influence IOF TGF-β2 levels. Received: 12 August 1996 Revised version received: 18 June 1997 Accepted: 18 July 1997     

外伤性白内障摘除人工晶体植入术后房水炎细胞研究

目的动态观察兔眼外伤性白内障囊外摘除及后房型人工晶体囊袋内植入术后早期炎症反应中房水细胞学动态变化．方法青紫兰兔27只，分为外伤性白内障晶体囊外摘除及后房型人工晶体囊内植入组，晶体囊外摘除组和正常对照组。术后d1、d3、d7和d14抽取房水计数白细胞总数及分类。采用SAS软件包，对统计资料作方差分析．结果外伤性白内障囊外摘除及后房型人工晶体囊袋内植入术组房水白细胞总数及各项分类计数明显高于单纯晶体囊外摘除组，差异有显著性．结论术后在d1房水白细胞总数、嗜中性粒细胞和嗜酸性粒细胞增加可能与手术所致的机械性创伤及血－房水屏障破坏有关，术后7～14d房水巨噬细胞增多可能是对人工晶体材料的一种免疫反应所致。     

Endotoxin-induced ocular inflammation increases prostaglandin E2 synthesis by rabbit lens

Twenty-four hours after the intravitreal injection of 0.1-100 ng of Escherichia coli endotoxin into one eye of the New Zealand white rabbit, lenses from the inflamed eyes synthesized significantly more prostaglandin E2 (PGE2) than their contralateral, control lenses at all doses of endotoxin greater than 0.1 ng. PGE2 elevations were also seen in the aqueous and vitreous humors from inflamed eyes. Lenses did not synthesize 6-keto-PGF1alpha (a stable metabolite of PGI2). Incubation of untreated lenses with 1 microgram ml-1 of endotoxin for 24 h did not increase PGE2 production. These results indicate that rabbit lens can synthesize PGE2, that this synthesis is significantly increased 24 hr after the intravitreal infusion of E. coli endotoxin, and that this increased PGE2 synthesis is most likely not due to a direct action of endotoxin on the lens.     

The influence of topical corticosteroid therapy upon polymorphonuclear leukocyte distribution, vascular integrity and ascorbate levels in endotoxin-induced inflammation of the rabbit eye

An acute inflammatory response was initiated in the rabbit eye by an intravitreal injection of bacterial endotoxin. We examined the effect of topical corticosteroid therapy upon polymorphonuclear leukocyte (PMN) infiltration into the eye, protein leakage into aqueous humor and ascorbate level in aqueous humor. Corticosteroid therapy initiated prior to injection of endotoxin suppresses the clinical signs of inflammation, partially prevents the fall in aqueous-humor ascorbate level, has little effect upon protein leakage, but markedly reduces PMN infiltration. Corticosteroid therapy initiated after the injection of endotoxin also suppresses the clinical signs of inflammation, reduces the fall in ascorbate levels and does not influence protein leakage. However, in this case there is a marked persistence of PMN infiltration into ocular tissues. Thus the number of PMNs present in the ocular tissues is little different from that in non-steroid treated control eyes, although the clinical signs of inflammation are reduced. We suggest that in the clinical situation, the initial anti-inflammatory activity of the corticosteroids is related to an inhibitory effect upon the activity of PMNs already within the tissues, which then prevents the ensuing cascade of characteristic inflammatory events.     

The effect of interleukin-1 on ocular inflammation in rabbit ocular tissue

IL-1 (Interleukin-1) has attracted attention not only as a mediator of the immunological response but as a substance involved in acute and chronic inflammatory responses. The author induced endophthalmitis by intravitreous injection of IL-1 into rabbit eyes. The inflammation model was characterized by the indicators of aqueous humor protein and PGE2 levels, and IL-1 and PAF were investigated as possible mediators of inflammation in IL-1 induced endophthalmitis. A prostaglandin (PG) synthetase inhibitor suppressed both the protein level and PGE2 level, while a PAF antagonist acted to inhibit the increase in the protein level in aqueous humor but did not inhibit the rise in PGE2. Combined administration of the PAF antagonist and the PG synthetase inhibitor further reduced both the protein and PGE2 levels. These findings suggest that PAF may be a mediator of endophthalmitis due to IL-1, and that IL-1 induced endophthalmitis is also modified by other factors in addition to PAF.     

PGE(2) and leucocyte levels in aqueous humor after lens extraction and intraocular lens implantation

In order to study the inflammatory response after cataract surgery and intraocular lens implantation the leukocyte (WBC) and prostaglandin E(2) (PGE(2)) levels in aqueous humor were measured in rabbit eyes at different time points (1, 3, 7, 14 and 28 days) postoperatively. In the first group lenses were implanted in the anterior chamber of the eye, without lens extraction, while in the second group the lens was removed and the IOL was placed in the capsular bag. A third group of animals was injected with 10 ng endotoxin into the vitreous in order to induce an inflammation of the uvea. In the endotoxin group high levels of WBC and PGE(2) were observed at 24 h postoperatively, followed by a decrease over time. In the intraocular lens groups WBC and PGE(2) were detected at all time points, and at higher levels compared to the endotoxin group. The WBC was high at day 1 and 3, declined over time, and then increased at day 28 postoperatively. The PGE(2) level was highest at day 3 in rabbits with anterior chamber lenses, while it peaked at day 7 in the animals with IOLs implanted in the capsular bag. In animals with the extracapsular lens extraction without an implanted IOL, the levels of WBC and PGE(2) decreased over time, and were statistically lower after one week compared with animals with an IOL placed in the capsular bag. The results demonstrate that the inflammatory response after cataract surgery persists for at least one month, probably due to surgical trauma and foreign body reactions. PGE(2) and WBC could be used to study postoperative trauma and biocompatibility of different IOL materials and designs.     

穿透角膜移植术后房水前列腺素E2及蛋白质量浓度的动态变化

目的　通过对穿透角膜移植术后房水前列腺素E2 (PGE2 )和蛋白质量浓度的测定 ,探讨PGE2 对炎症反应和免疫反应的作用。方法　 42只健康新西兰白兔 ,按穿透角膜移植术的类型和处理方法不同 ,随机分为 6组 ,分别于术后第 10、2 0、3 0、40d抽取各组动物的房水 ,用放射免疫法检测PGE2 质量浓度 ,用紫外分光光度计法测定蛋白质量浓度。结果　自体移植组术后 10d房水PGE2 质量浓度高于对照组 ;同种异体移植组术后 10、2 0d房水PGE2 质量浓度高于对照组 ,1只兔眼于术后 2 0d出现排斥反应 ;异种移植组术后 10、2 0、3 0d房水PGE2 质量浓度均高于对照组 ,有 6只兔眼于观察期内出现明显排斥反应 ;异种移植双氯芬酸钠和地塞米松 (DFNa Dex)治疗组术后 10d房水PGE2 质量浓度低于异种移植Dex治疗组(P <0 0 5 )。房水蛋白质量浓度的变化情况与PGE2 相一致。结论　PGE2 与穿透角膜移植术后的炎症反应和免疫排斥反应密切相关。Dex可抑制异种穿透角膜移植术后的排斥反应。DFNa对Dex有协同作用 ,可减少Dex的用量。     

兔眼IOL术后房水及泪液中白介素-8、钙离子的动态变化

目的研究晶状体超声乳化人工晶状体植入术（phaco＋IOL）及晶状体囊外摘出人工晶状体植入术（ECCE＋IOL）术后房水及泪液中自介素-8（IL-8）、钙离子（Ca^2＋）动态变化及其临床意义。方法30只青紫蓝家兔，随机分为3组（phaco＋IOL组，ECCE＋IOL组，正常对照组），每组10只。均为右眼。术后抽取房水和收集泪液。用比色法测定Ca^2＋，用放射免疫法测定IL-8。结果术后房水中IL-8活性第3天达高峰（P〈0．01），术后第3天Ca^2＋含量最低（P〈0．01）。术后各组泪液中IL-8术后第7天达高峰（P〈0．01），手术各组泪液中Ca^2＋在术后第3天达最低（P〈0．01）。房水与泪液中Ca^2＋、IL-8水平呈直线正相关（P〈0．05）．结论IL-8、Ca^2＋参与术后眼内炎症反应，检测泪液中IL-8和Ca^2＋的含量，能推断房水中IL-8、Ca^2＋含量，可作临床病情监测和指导用药的指标。