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Results for “Blood-Aqueous Barrier”

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At least 19 recordsLinked to original sources
PubMed1977

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.

Animals↗
PubMed1979

Sites of breakdown of the blood-aqueous barrier after paracentesis of the rhesus monkey eye.

Sites of breakdown of the blood-aqueous barrier following rapid paracentesis have been investigated in rhesus monkeys with two independent procedures. (1) The entrance of fluorescein into the anterior and posterior chambers following paracentesis was studied in vivo in normal eyes, in eyes with laser-induced experimental glaucoma, and in totally iridectomized eyes. (2) Scanning electron microscopy was used to study the ciliary body and trabecular meshwork regions in normal eyes and paracentetic eyes. These investigations show that the ciliary body, particularly the anterior pars plicata region, is a source of secondary aqueous humor protein. In addition, the study shows reflux of blood into Schlemm's canal and plasma movement across the inner wall into the anterior chamber.

Animals↗
PubMed1977

Ultrastructure of the blood-aqueous barrier in normal condition and after paracentesis A freeze-fracture study in the rabbit.

There is in the ciliary epithelium a barrier which prevents the passage of plasma proteins into the posterior chamber of the eye. The anatomical site of this blood-aqueous barrier is at the zonulae occludentes (tight junctions) located between the lateral plasma-membranes of the nonpigmented epithelial cells. Using the freeze-fracture technique we have studied these junctions in the pars plicata. As in many epithelia, they are formed by an anastomosing network of ridges on the fracture PF face and by a complementary set of furrows on the fracture EF face of plasma membranes. Features of these junctions are the presence of frequent parallel and closely associated double or triple ridges, and a few small gap junctions, associated with tight junctional elements of the zonulae occludentes. We also show that the number of junctional strands (ridges and furrows from apex to base) varies from a few strands to about 15, according to their position around the nonpigmented epithelial cells. These observations suggest that the rabbit's ciliary epithelium is to be classified among the 'tight' or 'very tight' epithelia (Claude and Goodenough, 1973). After paracentesis, we observed no breakdown of the zonulae occludentes. This supports the hypothesis that the site of leakage of the plasma proteins is elsewhere than ciliary epithelium.

Animals↗
PubMed1978

The blood-aqueous barrier and its permeability for proteins of different molecular weight.

In aqueous humors and sera from 44 patients with cataracts, albumin, IgG, and alpha-1-antitrypsin were measured using radial immunodiffusion. The mean concentrations of the three proteins were significantly smaller than values found in aqueous humors taken post mortem, but corresponded well to values found in cerebrospinal fluid. No statistically significant difference was found between men and women, normotensives and hypertensives, and patients with or without myopia of high degree (greater than 6 diopters). A slight increase in protein concentrations in older patients and a relative decrease of alpha-1-antitrypsin is described. The aqueous humor-serum quotients of the different proteins showed a higher correlation than did the concentration of the proteins in aqueous humors.

Aged↗
PubMed1979

Chronic degeneration of aminergic nerve endings and blood-aqueous barrier.

Chemical sympathectomy of the anterior segment of the eye was performed in rabbits with 6-hydroxydopamine (6-OHDA) intravitreously injected. The response of the pupillary diameter (PD) and intraocular pressure (IOP) to NE, E and Isoproterenol was determined through instillation of the drugs in the pretreated and control eyes. The results were as follows: 1) Both PD and IOP at different intervals of time from the injection show a sharp decrease in the treated eye. 2) About four weeks after the injection, the instillation of NE and E increases the PD only in the 6-OHDA pretreated eyes, while IP administration is not effective on both control and pretreated eyes. 3) The instillation of the three drugs, while decreasing IOP in the control eyes, does not modify the already low IOP in the pretreated eyes. The authors suggest the presence of a postdenervation supersensitivity affecting only the alpha receptors, since the beta stimulant IP is inactive in both treated and untreated eyes.

Animals↗
PubMed1979

Fluorescein angiography and changes in aqueous humor protein after argon laser photomydriasis in rabbits.

In brown-eyed and blue-eyed rabbits, irises treated with argon laser photomydriasis (ALP) were studied by using fluorescein angiography and by evaluating the aqueous humor protein concentration. The following results were obtained. Immediately after ALP, a breakdown of the blood-aqueous barrier is demonstrated by a marked influx of fluorescein into the ciliary processes and into the anterior and posterior chambers. The dye flow into the aqueous humor decreases to normal values within 3 days. There is no fluorescein leakage from laser impacts themselves. Peripupillary capillary loops are permanently occluded, but in a few cases, recanalization occurs. Neovascularization did not occur during 56 days of observation. ALP initially leads to a six- to eightfold increase in normal aqueous humor protein concentration, which decays to normal values within 3 days.

Animals↗
PubMed1977

Prevention of cystoid macular edema after lens extraction by topical indomethacin (I). A preliminary report.

Topically administered indomethacin was found to reduce the occurrence of cystoid macular edema after lens extraction. Indomethacin was given topically as 1% oil solution (sesame oil) eye drops twice or three times daily from the day before operation to the 40th day after operation. This effect suggests that prostaglandins play a leading role in the development of this disorder. It is postulated that operative irritation causes production of prostaglandins, which disrupt the blood-aqueous barrier, followed by an increase of the inflammatory mediators and debris in the aqueous. These inflammatory substances and prostaglandins themselves diffuse from the aqueous into the posterior pole of the fundus, where they induce inflammatory changes in vascular permeability in the perifoveolar capillary plexus. Clinically the cystoid macular edema then develops.

Administration, Topical↗
PubMed1979

Prostaglandin mediated inflammatory changes induced by alpha-adrenoceptor stimulation in the sympathectomised rabbit eye.

Topical application of 50 microliter of 0.1% noradrenaline or 10% phenylepherine to either a surgically sympathectomised or a guanethidine treated rabbit eye induced a transient increase in intraocular pressure (IOP), between 90 and 150 min, followed by a fall to hypotensive levels. These changes were accompanied by the development of conjunctival and anterior uveal hyperemia and an aqueous flare. Fluorescein angiography and microscopic examination after intravenously injecting colloidal carbon showed that the major site of disruption of the blood-aqueous barrier occurs in the ciliary processes. Slightly elevated levels of protein and prostaglandin-like activity (PG) were detected in aqueous samples withdrawn 3 or 5 h after application of either adrenergic agent. Prior treatment with indomethacin or phentolamine prevented the ocular hypertensive phase as well as the inflammatory changes, suggesting that the inflammatory rebound is mediated by PG and that PG release under such circumstances is closely linked to alpha-adrenoceptor activation. By contrast, the rise in IOP occurring after each of several successive daily applications of an alpha-agonist to a normal rabbit eye was not accompanied by hyperemia or an aqueous flare and was not inhibited by indomethacin pretreatment.

Animals↗
PubMed1977

Penetration of ocular compartments by tetracyclines. I. An experimental study with tetracycline.

Total antibiotic concentration of tetracycline hydrochloride was determined in the ocular structures of rabbits by radioactive tracer method. Concentration of tetracycline of 0.1 to 5 microgram/g, adequate to inhibit the growth of bacteria of high or medium susceptibility, was measured from all ocular structures with the exception of the lens. Tetracycline concentration in the aqueous humor was inferior to that in the vascularized ocular tissues and to that in the cornea. Vitreous body tetracycline level, about 0.3 microgram/g, was about half of the concentration in the aqueous humor. The disruption of the blood-aqueous barrier following paracentesis led to an immediate increase of tetracycline concentration in the anterior structures of the eye.

Animals↗
PubMed1979

Immediate changes in protein-concentration in aqueous humor induced by intracapsular lens extraction in human eyes.

In 71 patients that underwent intracapsular extraction of the cataract it was possible to collect aqueous humor (a.h.) in sufficient quantities at the beginning and at the end of the operation. Using radial immunodiffusion albumin, IgG and alpha-1-antitrypsin were measured in the samples. In secondary a.h. huge variations in the concentrations were apparent. The primary permeability of the blood-aqueous barrier and the time between sampling had no influence on the relative increase of the proteins. No statistically significant difference was found between normotensives and hypertensives and patients with or without myopia of higher degree (over 6 diopters). The relative increase of proteins according to their difference in molecular weight followed the same pattern as described for anterior uveitis. In patients for whom an enzymatic zonulolysis with trypsin was used for the extraction, the relative increase of IgG was significantly smaller than in those that did not receive this treatment (P less than 0.005). The possible sources contributing to the formation of secondary a.h. are discussed.

Aged↗
PubMed1976

Interaction of adrenergic antagonists with prostaglandin E2 and tetrahydrocannabinol in the eye.

Both alpha- and beta-adrenergic antagonists have been utilized in an atempt to discern the site of action of prostaglandin (PG) and tetrahydrocannabinol (THC) in the eye. Both alpha- and beta-adrenergic antagonists (alpha-antagonists, phentolamine and phenoxybenzamine; beta-antagonists, propranolol and sotalol) cuased a dose-dependent reduction in intraocular pressure and blood pressure and increased total outflow facility. The results are consistent with the concept that both alpha- and beta-adrenergic receptors are present in the anterior uvea and that vasomotor tone is essential to the maintenance of normal intraocular pressure. No antagonist reduced the PG-induced elevation of intraocular pressure unless the blood pressure was severely lowered. All antagonists inhibit the normal PG-induced increase in total outflow facility, indicating that these agents protect the blood-aqueous barrier from breakdown without altering the vasodilatory response to PG. All antagonists reduced the fall in intraocular pressure produced by THC by approximately 50 per cent, except for sotalol which completely abolished the intraocular pressure fall. Only the alpha-adrenergic antagonists prevented the THC-induced increase in total outflow facility. The results indicate that true outflow facility may well be regulated exclusively by alpha-receptors. The data are consistent with the effect of THC being primarily a vasodilation of the efferent blood vessels of the anterior uvea. The partial inhibition by alpha-adrenergic antagonists may also suggest a lesser role of THC on the afferent vessels.

1-Propanol↗
PubMed1976

Prostaglandins, nonsteroidal anti-inflammatory agents and eye disease.

The prostaglandins produce elevation of intraocular pressure and breakdown of the blood-aqueous barrier. They act via the secondary messenger system, cyclic AMP. Although the pathogenesis of many forms of ocular inflammation, both external and internal, is unclear, it is evident that some forms of ocular inflammation are prostaglandin-mediated, at least in part. Others may be totally mediated by prostaglandin synthesis. At present the corticosteroids are the mainstay of therapy of these conditions. However, the corticosteroids are poor inhibitors of prostaglandin synthesis and have many deleterious side effects such as induction of ocular hypertension, cataract, and infection. The search for new agents that will obviate these side effects and be more specific for the disease process is crucial. The discovery that the mode of action of many nonsteroidal anti-inflammatory agents is via inhibition of prostaglandin synthesis places a premium on elucidating which of these agents is most effective and least toxic in the eye and by which route of administration. The arachidonic acid screening model is ideal for initially choosing which agent has the greatest potential clinically. Arachidonic acid, a PGE2 precursor, when given topically also elevates intraocular pressure and aqueous humor protein, and these effects are blocked by the nonsteroidal anti-inflammatory drugs. This occurs if the arachidonic acid is injected into the vitreous humor, too, providing evidence that this in vivo model involves intraocular mechanisms. Utilizing the arachidonic acid system, a comparative study of nonsteroidal inhibitors of prostaglandin synthesis shows that the most effective of 14 agents were flurbiprofen solution and suspensions of polysorbate-dispersed indoxole, meclofenamic acid, indomethacin, and clonixin. Animal uveitis is not an ideal model for the human condition. Nevertheless, proving the superior efficacy of a screened drug in this system will identify those drugs to be tested in the human disease states. Only after the very few best drugs of this nature are identified should the ultimate steps of human testing be initiated.

Animals↗
PubMed1977

Hyperproduction glaucoma.

Hyperproduction glaucoma is a tonographic clinical entity characterized by high IOP and normal C: 1. It may occur as open angle glaucoma spontaneously or pharmacologically induced. 2. It may be an inflammatory ocular hypertension characterized by a breakdown of the blood-aqueous barrier. The treatment of choice is topical and/or systemic drugs such as epinephrine and acetazolamide which inhibit aqueous inflow; glucocorticoids should be added in cases of the inflammatory type. The pathogenesis is directly related to hyperproduction of aqueous, depending chiefly on increased capillary hydrostatic pressure at the level of the ciliary body.

Aqueous Humor↗
PubMed1978

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.

Animals↗