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Query: UMLS:C0595921 (intraocular pressure)
 11,750 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Topical administration of aqueous solutions of sodium arachidonate to the eyes of rabbits increases intraocular pressure, constricts the pupil and increases both the protein and prostaglandin content of aqueous humor. Arachidonic acid itself dissolved in arachis oil is less effective than sodium arachidonate, although addition of polysorbate mono-oleate greatly increases the effects produced by arachidonic acid. Pretreatment with topically applied non-steroidal anti-inflammatory agents prevents the ocular effects of sodium arachidonate, indomethacin being 2-4 times as potent as either indoxole or pirprofen. Dexamethasone was without effect in these experiments. The results suggested that nonsteroidal anti-inflammatory agents deserve serious consideration for topical use in the treatment of ocular inflammation.
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PMID:Inhibition of the ocular effects of sodium arachidonate by anti-inflammatory compounds. 113 34

Arachidonic acid, a precursor of prostaglandin E2 subconjunctivally injected into rabbit eyes in concentrations of 0.8 to 5 per cent, produced a dose-related rise of intraocular pressure (IOP) similar to the one observed after topical administration of PGE2 in concentrations of 0.001 to 0.1 per cent. Indomethacin, a nonsteroidal anti-inflammatory agent, had an inhibitory effect when administered systemically or topically prior to arachidonic acid. Dose-response relationships were demonstrated by topical and oral administration of Indomethacin which, as expected, had no effect on PGE2. Dexamethasone did not exert any inhibitory effect on the increased IOP following arachidonic acid administration. Indomethacin applied topically readily penetrated into the aqueous humor in concentrations considerably above those appearing in the plasma, which justifies the use of this route of administration. Since prostaglandin (PG) appeared to be implicated in ocular inflammation, these findings underline the specificity of action of Indomethacin and suggest its use in the topical treatment of ocular inflammation.
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PMID:Arachidonic acid-induced elevation of intraocular pressure and anti-inflammatory agents. 118 10

Topical dexamethasone was used to elevate rabbit intraocular pressure in order to study the interaction with a steroid antagonist, mifepristone. Dexamethasone did not cause a consistently significant increase in intraocular pressure. Animals treated with mifepristone followed by dexamethasone showed no apparent increase in intraocular pressure after dexamethasone, indeed mifepristone caused a lower intraocular pressure than seen in other groups whether in the presence or absence of dexamethasone. Reductions of intraocular pressure when mifepristone was given after 14 days of dexamethasone administration were not found. No conclusion can be reached regarding any dexamethasone antagonism by mifepristone, except that intraocular pressure tended to be lower even in the presence of dexamethasone.
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PMID:Effects of mifepristone on rabbit intraocular pressure in the presence and absence of dexamethasone. 208 41

5 beta-dihydrocortisol potentiates the action of topically applied dexamethasone in raising the intraocular pressure (IOP) in young rabbits. Dexamethasone (0.06%) plus 5 beta-dihydrocortisol (0.1 and 1.0%) elevated the IOP 7-10 mmHg within 18 days of treatment. By contrast, 0.06% dexamethasone alone raised the IOP 3 to 4 mmHg in a similar period of time. Since 5 beta-dihydrocortisol accumulates abnormally in cultured cells derived from the outflow region of the eye from patients with primary open angle glaucoma (POAG), a similar potentiation in man may account for the sensitivity of these patients to the IOP raising effect of glucocorticoids. Further, this metabolite may potentiate endogenous glucocorticoids resulting in the ocular hypertension characteristic of POAG.
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PMID:5 beta-Dihydrocortisol: possible mediator of the ocular hypertension in glaucoma. 397 22

We studied the effect of suprofen, a new ophthalmic nonsteroidal anti-inflammatory agent, on corneal wound healing. Nine-millimeter, central, perforating corneal wounds were made in albino rabbits and sutured with 10-0 nylon. The animals were randomly treated with balanced salt solution, suprofen vehicle, 1% suprofen, or 0.1% dexamethasone sodium phosphate administered topically for six days. On the seventh postoperative day, the sutures were removed and, in situ, the intraocular pressure was increased in a controlled manner until the wound burst. Dexamethasone applied four times a day significantly inhibited corneal wound healing, whereas suprofen given as often as hourly did not. Pretreatment with hourly administered suprofen for two days prior to surgery, in addition to the same postoperative hourly therapy, also did not significantly decrease stromal wound strength.
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PMID:Effect of suprofen on corneal wound healing. 397 82

A clinical double-blind study of patients who had undergone intracapsular cataract extraction with intraocular implant was performed in an attempt to compare the anti-inflammatory effect of Dexamethasone and Diclofenac eye drops. The parameters compared were: degree of inflammation of the anterior chamber; pachymetry of the cornea; objective and subjective tolerance of the eye drops; examination of the fundus (fluorescein angiography on the 60th day); intraocular pressure. The statistical analysis of the different parameters shows a tendency in favor of the non-steroidal agent for intraocular pressure; there was no apparent difference in the anti-inflammatory actions of the two substances.
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PMID:[Comparison of the anti-inflammatory effect of collyria of dexamethasone and diclofenac]. 637 74

Further studies have been made with water soluble marihuana-derived material (MDM). Neither adrenergic, cholinergic, aldosterone, dopamine or serotonin antagonism affected the fall in intraocular pressure induced by MDM. Partial blockade was obtained with galactose, glucose, or mannose, but not arabinose, when the latter were given at intravenous concentrations of 1 gm/animal and MDM was given at 25 micrograms animal, suggesting that these sugars may be involved at the active site of the MDM glycoproteins. Dexamethasone was without effect on either intravenous or intravitreal MDM indicating that the MDM effect is not a non-specific response to a protein. A similar plant glycoprotein, larch arabinogalactan, at 200 micrograms/animal was without effect on intraocular pressure. Aqueous humor flow rate was increased 3 hours after MDM administration, a period corresponding to the intraocular pressure increase caused by MDM, and fell to 20% of control values when the fall in intraocular pressure occurred. Blood flow through the iris was increased at both one and six hours after intravenous MDM injection indicating a vasodilation which could contribute to the initial increase in intraocular pressure. Intravitreal injection of MDM in rabbit and rhesus monkey caused a fall in intraocular pressure only after a 24 hour delay: the unilateral response indicated that systemic metabolism was not required for activity and the delay was likely caused by the diffusion time to the ciliary processes from the mid-vitreal injection site. The changes in beta-receptors, adenylate cyclase and carbonic anhydrase in the ciliary processes are minimal indicating a possible vascular mechanism of action of MDM.
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PMID:Water soluble marihuana-derived material: pharmacological actions in rabbit and primate. 734 31

The group of 60 patients suffering from chronic non-infected reaction of conjunctivits, showing irritation, conjunctival hyperemia, pain and photophobia, have been treated in the open observational clinical trial comparing the efficiency, safety and local tolerance of diclofenac sodium eye drops 0.1% (Naclof) versus dexamethasone eye drops (Dexamethasone oph. 0.1%) during a period of 30 days. Both medications were locally well tolerated. Naclof caused some slight temporary burning slightly more frequently than dexamethasone but the difference was not statistically significant (Naclof 89.7% tolerability and Dexamethasone 89.1% tolerability). The two drugs were equally effective in the treatment of chronic non-infected conjunctivitis. All the patients have shown a gradual improvement of the symptoms as well as of the objective sings. The dexamethasone group showed an increase in intraocular pressure at the third and fourth visit. However, these differences are not statistically significant either.
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PMID:[Naclof in the treatment of chronic non-infectious conjunctivitis]. 865 25

The functional significance of Hyaluronan (HA) present in the cribriform layer of Schlemm's canal is not known. It may contribute to the actual outflow resistance but the relatively inert molecule might also be necessary to prevent adherence of larger molecules to the cribriform network. Thus HA might rather prevent an increase in outflow resistance. It is well known that treatment with Dexamethasone (DM) in a number of patients leads to an increase in intraocular pressure presumably due to an increase in outflow resistance. To clarify whether an imbalance in HA formation might be involved in these changes we have treated confluent cultures of human trabecular cells as well as control cell lines (ciliary muscle cells, scleral fibroblasts) with 500 nM DM for 24 hr or 12 days and have measured HA-synthesis using incorporation assays with 0.05 m D-[6-3H] Glucosamine hydrochloride. In all six cell lines investigated there was a significant decrease in HA-synthesis following short and long term treatment with DM when compared with the untreated controls. This reaction of trabecular cells to DM treatment is different from the DM effect reported on the synthesis of many other components of the extracellular matrix like fibronectin and elastin which increase after DM treatment. If the DM-effect seen in cell cultures plays a role in vivo decreased formation in HA could result in impaired function of the outflow pathways.
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PMID:Dexamethasone treatment decreases hyaluronan-formation by primate trabecular meshwork cells in vitro. 922 71

The trabecular meshwork forms most of the resistance to aqueous humor outflow needed for maintenance of a pressure gradient between intraocular pressure of approximately 17 mmHg and venous pressure of approximately 10 mmHg. The composition of the extracellular material in the subendothelial or cribriform layer seems to be mainly responsible for outflow resistance. The aqueous humor pathways through the subendothelial layer can be influenced by ciliary muscle contraction and presumably also by contractile elements recently found both in trabecular meshwork and scleral spur. Pharmacologically induced disconnection of inner wall and cribriform cells leads to wash out of extracellular material through breaks of the endothelial lining of Schlemm's canal and to increase of outflow facility. In glaucomatous eyes the resistance to aqueous humor outflow is increased due to an increase in different forms of extracellular material deposited within the cribriform layer. The amount of this newly developed extracellular material is correlated with loss of axons in the optic nerve, indicating that a common factor is responsible for both changes. To investigate the effect of various factors on the biology of trabecular cells monolayer cultures derived from cribriform and corneoscleral trabecular meshwork have been established. The two cell lines can be differentiated because cribriform cells in vivo as in vitro stain for alphabeta-crystallin whereas the corneoscleral cells remain unstained. The effect of TGFbeta, a growth factor increased in aqueous humor of glaucomatous eyes and glycocorticoids on trabecular meshwork cells show typical changes in formation of extracellular matrix components and of stress proteins. Dexamethasone and oxidative damage also lead to increase of trabecular meshwork inducible glucocorticoid response (TIGR) protein. A mutation of the TIGR-gene family has recently been found in families with juvenile and chronic simple glaucoma. Future research has to clarify the significance of these genetic factors for the pathophysiology of glaucoma and the role of trabecular cell activity in this respect.
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PMID:Functional morphology of the trabecular meshwork in primate eyes. 992 May


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