Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0595921 (intraocular pressure)
 11,750 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the ability of rabbit ciliary epithelium to metabolize arachidonic acid in vitro. The epithelium was homogenized and incubated with 14C-labeled arachidonic acid. 14C-labeled metabolites were extracted and then separated by thin layer chromatography. The range of arachidonic acid metabolites synthesized by ciliary epithelium was compared to the metabolites generated by rabbit iris-ciliary body. Ciliary epithelium produced substantial amounts of arachidonic acid metabolites that comigrated with 5-HETE and 12-HETE. Authenticity of the 12-HETE produced by ciliary epithelium was confirmed by gas chromatography/mass spectrometry. The ciliary epithelium generated only small amounts of the cyclooxygenase products, PGF2 alpha, PGE2, PGD2 and 6k-PGF1 alpha. In contrast, the iris-ciliary body produced large amounts of cyclooxygenase products such as PGF2 alpha and PGD2. The ability of the ciliary epithelium to generate 12-HETE is noteworthy since 12(R)-HETE is known to be capable of lowering intraocular pressure.
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PMID:Metabolism of arachidonic acid by isolated rabbit ciliary epithelium. 142 59

An inflammatory response was elicited in the rabbit eye by intracameral injection of platelet activating factor (PAF). PAF induced severe aqueous flare, corneal edema, pupillary constriction and marked biphasic changes in intraocular pressure (IOP) in a dose-dependent manner. All of the responses to PAF were inhibited by the PAF receptor antagonist, BN 52021 (20 mg/kg, i.p.). The cyclooxygenase inhibitor, indomethacin (30 mg/kg, i.p.) caused significant inhibition of the early phase PAF-induced aqueous flare, pupillary constriction and intraocular hypertension, but did not effect PAF-induced corneal edema or intraocular hypotension. NDGA (10 mg/kg, i.p.), a lipoxygenase inhibitor, did not inhibit the inflammatory effects of PAF. PAF-induced chemotactic response was evaluated by tissue chemiluminescence. Intracamerally injected PAF did not significantly increase chemiluminescence in cornea or iris-ciliary body, but intracorneal injection of PAF did cause a chemotactic response in both the conjunctiva and cornea. These data suggest that PAF may be an important mediator of intraocular inflammation and that some PAF-induced effects are prostaglandin dependent, while others may be independent of eicosanoid synthesis and release.
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PMID:Intracamerally injected platelet activating factor (PAF) induces marked intraocular inflammatory reactions. 148 37

Cod liver oil administered intramuscularly (0.2 ml/day) lowered intraocular pressure (IOP) of the rabbit from 21 mmHg to 18 +/- 0.4 mmHg (p less than 0.05 n = 8). A higher dose of cod liver oil (1 ml) further lowered intraocular pressure to 14.5 +/- 0.3 mmHg which remained at this level for up to 80 days when the rabbits were sacrificed. Intramuscular injections of liquid lard did not alter IOP in rabbits. When treatment with cod liver oil was stopped, IOP rose to baseline levels. Topical treatment with cyclooxygenase inhibitors had no effect on the IOP lowering effect of cod liver oil. Topical treatment of rabbit eyes with 1% aspirin solution twice daily (up to 28 days) and flurbiprofen t.i.d. (up to 15 days) caused no alteration in the decrease in IOP seen with intramuscular cod liver oil treatment for up to 28 and 15 days respectively.
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PMID:A comparative study between cod liver oil and liquid lard intake on intraocular pressure on rabbits. 158 51

Sodium naproxen, a reversible competitive inhibitor of cyclooxygenase, is widely used as an anti-inflammatory agent in clinical practice. The purpose of this study was to determine whether eye drops containing 0.5% (w/v) sodium naproxen reduce a number of inflammatory responses produced by sodium arachidonate in the rabbit's eye. Sodium naproxen eye drops successfully reduced the primary signs of ocular inflammation elicited by 0.5% sodium arachidonate on conjunctiva and iris. However, the drug was less effective in reducing conjunctival inflammation induced by 1% sodium arachidonate. Sodium naproxen treatment significantly reduced the levels of prostaglandin E2 (PGE2), polymorphonuclear leukocytes and protein concentration in aqueous humor samples obtained from the eyes of rabbits treated with 0.5% sodium arachidonate whereas aqueous humor levels of leukotriene B4(LTB4) were not found significantly different from control rabbits. Interestingly, PGE2 as well as LTB 4 "de novo" production by corneas and lenses obtained from rabbits sacrificed 2 h after arachidonate and incubation "in vitro" for 20 min were significantly higher in samples taken from controls than in tissues obtained from the eyes treated with sodium naproxen eye drops. Finally, this drug treatment significantly antagonized the rise in intraocular pressure induced by 0.5% sodium arachidonate. Present data suggest that sodium naproxen may be employed topically to prevent ocular inflammatory reactions where the arachidonic acid cascade is activated.
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PMID:Effects of sodium naproxen eye drops on rabbit ocular inflammation induced by sodium arachidonate. 165 31

Ocular inflammation was induced in 36 dogs by performing an anterior capsulotomy with a Nd:YAG laser. All dogs were pretreated with topical atropine. Dogs were then divided into three groups: (1) control, with no other pretreatment; (2) pretreatment with the topical dual cyclooxygenase/lipoxygenase inhibitor RMI-1068; and (3) pretreatment with topical prednisolone acetate. Dogs were studied 1-3 hours after lasering. RMI-1068 maintained mydriasis and raised intraocular pressure compared to the control and prednisolone groups. An ocular fluorophotometer used to measure anterior chamber fluorescence after IV injection of sodium fluorescein showed that RMI-1068 decreased anterior chamber fluorescein concentration compared to the control and prednisolone groups. RMI-1068 decreased PGF2 alpha concentrations in the aqueous at 1 and 3 hours compared to the control and prednisolone groups. Prednisolone decreased PGF2 alpha concentrations compared to the control group at 1 h. Concentrations of LTB4 in the aqueous at 1 hour were lower in the RMI-1068 group than in the control and prednisolone groups.
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PMID:Comparison of prednisolone and RMI-1068 in the ocular irritative response in dogs. 174 Mar 79

After argon trabeculoplasty procedures in patients with chronic open angle glaucoma, the protein appearance and cell circulation were observed within the anterior chamber. Flare and cell measurements of the anterior compartment are parameters of aqueous blood barrier break down. This investigation was performed in 50 patients suffering from elevated intraocular pressure and treated with argon laser trabeculoplasty. Two different anti-inflammatory drugs (prednisolone acetate and cyclooxygenase inhibitor) were applied to the treated eyes and checked for their effect on inflammation reduction. The protein and cell concentrations within the anterior chamber were measured before and 6 and 24 h after trabeculoplasty with a flare cell meter (KOWA) and compared to a control group. Argon laser trabeculoplasty induces an increase in protein concentration within the anterior chamber. This investigation demonstrates a clear drop in the inflammatory reaction of treated eyes during prednisolone acetate and cyclooxygenase inhibitor application. The intraocular pressure was reduced to about 6 mm Hg in treated eyes from an average pressure of 26 mm Hg.
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PMID:[Anti-inflammatory treatment after argon laser trabeculoplasty]. 143 92

Experiments were undertaken in normal albino rabbits to determine if cyclooxygenase inhibition by nonsteroidal anti-inflammatory drugs modified the ocular hypotensive activities of topically applied MK-507, MK-927 and L-662,583, three water-soluble carbonic anhydrase inhibitors (CAI). Cyclooxygenase was inhibited either by systemic indomethacin or by topically administered flurbiprofen, and epinephrine was included as a positive control. Both a 1-hr pretreatment with indomethacin (5 mg/kg i.p.) and topically applied 0.03% flurbiprofen antagonized the ocular hypotensive effect of one drop (50 microliters) of 1% epinephrine. Two percent solutions of the three CAIs were instilled three times with 10 min between each drop in order to obtain a meaningful and reproducible reduction in intraocular pressure (IOP). This dosage schedule elicited a peak decline in IOP ranging from 4.6 mm Hg to 6.2 mm Hg which was achieved via a local action within the eye. The ocular hypotensive effects of MK-507, MK-927 and L-662,583 were unaltered either by a 1-hr pretreatment with indomethacin (5 mg/kg i.p.) or by topically administered 0.03% flurbiprofen. These studies indicate that the IOP lowering actions of the three CAIs, unlike that of epinephrine, in rabbits are not mediated by endogenous prostaglandins and/or other prostanoids.
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PMID:The effect of cyclooxygenase inhibition on the ocular hypotensive action of topical carbonic anhydrase inhibitors in rabbits. 178 53

In rabbits, laser irradiation of the iris causes an immediate rise in intraocular pressure (IOP), with a concomitant increase of prostaglandins (PGs) in the aqueous humor. We studied IOP responses to Q-switched Nd:YAG laser application to the iris in unanesthetized rabbits, and found that a prolonged IOP reduction lasting for 6-24 hr invariably followed the transient IOP rise of 0.5-2 hr duration. The magnitude of both the IOP rise and reduction was dependent on the level of laser energy. A masked, randomized study revealed that the intraperitoneal administration of indomethacin (50 mg kg-1) prior to laser application significantly reduced the ocular hypertensive and hypotensive responses to laser irradiation (energy: 24 mJ). The maximum IOP rise from baseline was 5.4 +/- 3.0 mmHg (n = 10) with the intraperitoneal vehicle and 1.5 +/- 4.2 mmHg (n = 10) with intraperitoneal indomethacin administration. Thus, the difference was statistically significant (P less than 0.025, Student's t-test). The maximum IOP reduction from baseline was -8.5 +/- 2.6 mmHg (n = 10) with the intraperitoneal vehicle and -4.0 +/- 2.4 mmHg (n = 10) with intraperitoneal indomethacin (P less than 0.001, Student's t-test). The concentration of PGE2 in the aqueous humor, as determined by radioimmunoassay on samples obtained at 2 and 4 hr after laser application, was found to be significantly increased in rabbits that received the vehicle solution but not in animals that were pretreated with intraperitoneal injection of indomethacin. This suggests that this PG or other cyclooxygenase products are involved with mediation of the initial IOP increase and the prolonged decrease in IOP that follows laser irradiation of the iris.
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PMID:Biphasic intraocular pressure response to Q-switched Nd:YAG laser irradiation of the iris and the apparent mediatory role of prostaglandins. 224 28

Topical adrenaline lowers intraocular pressure (IOP) in the rabbit largely due to an increase in facility of outflow of aqueous humour. This paper studies the inhibition by indomethacin or piroxicam of the adrenaline-induced rise in facility of outflow. Topical indomethacin is shown to reduce the acute IOP changes induced by adrenaline in conscious rabbits; both the early rise and the prolonged fall in pressure were inhibited. In anaesthetized rabbits, indomethacin pretreatment prevented the large rise in facility of outflow which normally follows topical adrenaline. Indomethacin did not block the mydriasis induced by adrenaline, nor did it significantly alter aqueous humour protein levels. Piroxicam, a cyclo-oxygenase inhibitor which, unlike indomethacin, does not block Ca2+ movements in some tissues, also blocked the adrenaline-induced rise in facility of outflow, suggesting that this increased facility depends on cyclo-oxygenase and not on Ca2+ movements. Verapamil, a drug which blocks Ca2+ channels, was shown to inhibit the brief ocular hypertensive effect of adrenaline in the conscious rabbit, but to leave the hypotensive phase unchanged. It is concluded that the hypotensive mechanism of adrenaline may depend on synthesis of a prostaglandin, since inhibition of the adrenaline-induced rise in facility is achieved by inhibitors of cyclooxygenase. Despite previous reports that a prostaglandin may be responsible for the brief hypertensive phase, the present evidence suggests that Ca2+ movements may be involved, perhaps in activation of the extraocular muscles.
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PMID:Inhibition by indomethacin of the increased facility of outflow induced by adrenaline. 231 77

Pathways of arachidonic acid metabolism were identified in freshly prepared and in cultured bovine corneal endothelial cells. The principal pathway of arachidonic acid metabolism in the bovine corneal endothelial cells appears to be the cyclooxygenase pathway with the resultant synthesis of PGI2, PGF2 alpha and PGE2. At least two of these products, PGI2 and PGF2 alpha, are formed by the enzymatic conversion of the substrate, PGH2. Measurements of endogenous prostaglandin production by radioimmunoassay demonstrated that PGE2 was the major arachidonic acid metabolite released, with smaller amounts of PGF2 alpha and the stable hydrolysis product of PGI2, 6-keto PGF1 alpha. The release of all three prostanoids was significantly increased by the addition of the calcium ionophore (A23187), human thrombin, bradykinin and histamine. Basal and stimulated release of prostaglandins by the corneal endothelium may contribute to the regulation of intraocular pressure and also in the modulation of the corneal response to injury.
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PMID:Arachidonic acid metabolism by cultured bovine corneal endothelial cells. 249 58


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