Disease relevance of Blood-Aqueous Barrier

• None of the antagonists could inhibit the miosis or disruption of the blood-aqueous barrier induced by topical neutral formaldehyde [1].
• Latanoprost accelerates disruption of the blood-aqueous barrier and the incidence of angiographic cystoid macular edema in early postoperative pseudophakias [2].
• CONCLUSIONS: Timolol and its preservative, benzalkonium chloride, cause disruption of the blood-aqueous barrier in early postoperative pseudophakia and increased incidence of angiographic CME [3].
• Effect of indomethacin and prednisolone on the disruption of the blood-aqueous barrier after hyperthermia on the rabbit eye by focused ultrasound [4].
• The blood-aqueous barrier in anisometropia and high myopia [5].

High impact information on Blood-Aqueous Barrier

• The intravitreal injection of 10(5) to 5 X 10(5) units of recombinant human TNF produced a sustained disruption of the blood-aqueous barrier as manifested by elevated aqueous humor protein levels [6].
• The status of the blood-aqueous barrier correlated significantly with serum CHO and TG levels (r = .46, P < .001; r = .23, P = .01, respectively) [7].
• Changes in the blood-aqueous barrier function associated with total serum cholesterol (CHO) and triglyceride (TG) levels were studied at the beginning of the study and every 2 weeks thereafter for up to 16 weeks following 0.5% cholesterol-enriched diet feeding [7].
• The lack of an IOP response in the FP-knockout mice was not a consequence of blood-aqueous barrier breakdown, as there was no significant difference in aqueous humor protein concentration between treated and fellow eyes [8].
• Blood-aqueous barrier function was studied measuring aqueous protein and fluorescein concentration after intravenous dye injection [9].

Chemical compound and disease context of Blood-Aqueous Barrier

• OBJECTIVES: To investigate the effects of prostaglandin analogues on the blood-aqueous barrier and to evaluate the occurrence of cystoid macular edema in aphakic or pseudophakic patients with glaucoma [10].
• Recent clinical studies indicate that flurbiprofen, a cyclooxygenase inhibitor, prevents miosis and breakdown of the blood-aqueous barrier during cataract surgery [11].
• Following YAG-laser anterior capsulotomy, captopril inhibited the increase in IOP, breakdown of the blood-aqueous barrier and miosis [12].

Biological context of Blood-Aqueous Barrier

• The effect of thymoxamine on intraocular pressure and anterior chamber volume was also studied. four of the 25 subjects were used to study the effect of thymoxamine on the permeability to fluorescein of the blood-aqueous barrier [13].
• In the eye, prostaglandins (PGs), in particular PGE2 and PGF2 alpha, may induce vasodilation, disruption of the blood-aqueous barrier, and biphasic effects on intraocular pressure, depending on the species [14].
• Thus, although LTD4 increased conjunctival microvascular permeability, it does not appear to disrupt the blood-aqueous barrier of the guinea pig eye [15].
• The effects of sensory nerve stimulation (topical neutral formaldehyde, 1%) and intracameral injection of calcitonin gene-related peptide (CGRP) on regional ocular blood flow, intraocular pressure (IOP), the blood-aqueous barrier, pupil size, and blood pressure were studied in the rabbit [16].
• The predominant distribution of PGE2 binding sites in the ciliary body and their identification as EP2 selective, supports recent functional studies where topical application of prostanoids with EP2 but not EP1 or EP3 agonist activity resulted in breakdown of the blood-aqueous barrier [17].

Anatomical context of Blood-Aqueous Barrier

• All 26 received topical fluorescein to determine the anterior chamber elimination coefficient; five received systemic fluorescein to evaluate the integrity of the blood-aqueous barrier [18].
• Intraocular lidocaine in phacoemulsification: an endothelium and blood-aqueous barrier permeability study [19].
• A reversible breakdown of the blood-aqueous barrier in the iridial processes of rabbits has been induced by arachidonic acid as demonstrated by the passage of horseradish peroxidase at places through the tight junctions [20].
• Arachidonic acid induced a reversible breakdown of the blood-aqueous barrier in the iridial processes of the rabbit ciliary body, whereas the ciliary processes were not affected under the conditions of this study [21].
• The exact sites of the blood-aqueous barrier, demonstrated by tracing the acriflavine fluorescence through tissues and individual cells, were in the basal cell membranes of inner ciliary and iridial epithelia and apical cell membranes of iridial and corneal endothelia [22].

Associations of Blood-Aqueous Barrier with chemical compounds

• Prolonged monitoring of the blood-aqueous barrier with fluorescein-labeled albumin [23].
• 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) [24].
• The increase in IOP as well as the breakdown of the blood-aqueous barrier could not be blocked with TTX or indomethacin [25].
• The results indicate that all three stimuli tested are at least partly dependent upon an intact sensory innervation to disrupt the blood-aqueous barrier, but that the mechanism of action of PGE2 is different from that of IR and alpha-MSH [26].
• The effect of timolol maleate on the disruption of the blood-aqueous barrier in the rabbit eye [24].

Gene context of Blood-Aqueous Barrier

• VEGF-induced blood-retinal and blood-aqueous barrier breakdown was completely blocked by the corticosteroid DEX administered systemically for 3 days [27].
• CGRP-II caused a monophasic increase in the IOP and disruption of the blood-aqueous barrier, but no increase in the cAMP content occurred [28].
• The ciliary processes and iris revealed an identical transferrin pattern as in the serum. alpha 2-Macroglobulin, that has been thought to be too large to pass the blood-aqueous barrier, was detected in all of the aqueous humor samples [29].
• CONCLUSIONS: During corneal graft rejection and/or HSV-infection, increased levels of TP and IL-6 in AH confirmed anterior chamber inflammation with breakdown of the blood-aqueous barrier [30].
• Localization of GLUT1 and connexin 43 in the blood-aqueous barrier suggests that GLUT1, connexin 43, and GLUT1 disposed in this order could be a machinery responsible for the transport of glucose across the blood-aqueous barrier [31].

Analytical, diagnostic and therapeutic context of Blood-Aqueous Barrier

• CONCLUSION: Argon laser trabeculoplasty produces a greater disruption of the blood-aqueous barrier than DLT [32].
• We studied the effects of visible (400-750 nm), infrared (750-1100 nm), and ultraviolet (300-400 nm) radiation on the breakdown of the blood-aqueous barrier (BAB) in albino rabbit eyes using fluorophotometry and fluorescein-bound albumin [33].
• PURPOSE: To evaluated the influence of heparin-surface-modified (HSM) versus unmodified poly(methyl methacrylate) (PMMA) intraocular lenses (IOLs) on the blood-aqueous barrier (BAB) in at-risk eyes [34].
• The transport of [3H] adenosine and [3H] thymidine across the blood-aqueous barrier proved to be very rapid with a volume of distribution after 4 minutes perfusion reaching 11.9+/-3.0% and 9.93+/-1.1%, respectively [35].
• Quantification of blood-aqueous barrier breakdown after photorefractive keratectomy for myopia [36].

References