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1 ty but has no effect on aqueous secretion or uveoscleral outflow.
2 ated with lower aqueous production and lower uveoscleral outflow.
3 tes the possibility that brimonidine affects uveoscleral outflow.
4 l PG treatment could contribute to increased uveoscleral outflow.
5 may thus indicate a drug-induced increase in uveoscleral outflow.
6 intraocular pressure primarily by enhancing uveoscleral outflow.
7 t night is counterbalanced by an increase in uveoscleral outflow.
8 Gs) lower intraocular pressure by increasing uveoscleral outflow.
9 ressure has led to increased interest in the uveoscleral outflow.
10 ular pressure (IOP), primarily by increasing uveoscleral outflow.
12 mportant information about the regulation of uveoscleral outflow and the pathologic course of glaucom
14 crease aqueous humour production or increase uveoscleral outflow by different mechanisms from those d
17 iliary muscle cells has a role in increasing uveoscleral outflow facility after topical PG administra
18 liary muscle ECM may contribute to increased uveoscleral outflow facility after topical PG administra
19 liary muscle ECM may contribute to increased uveoscleral outflow facility during anterior segment inf
20 supporting the hypothesis that increases in uveoscleral outflow facility induced by PG administratio
21 increased MMPs contributing to the increased uveoscleral outflow facility observed after topical lata
26 ing the vortex veins did not appear to alter uveoscleral outflow further (1.2 +/- 0.8 microL/min).
27 dertaken to assess directly whether there is uveoscleral outflow in the mouse eye by monitoring the m
28 and endothelin (ET)-1, induce an increase in uveoscleral outflow, in part through receptor-mediated m
29 traocular pressure, presumably by increasing uveoscleral outflow induced by relaxation of the CM.
30 ynamics (aqueous flow, outflow facility, and uveoscleral outflow), IOP, and pachymetry data from 94 h
35 contributes to regulation of MMP within the uveoscleral outflow pathway after exposure to latanopros
36 ent of normal human eyes associated with the uveoscleral outflow pathway and in the iris, corneal end
37 HCM cells could contribute to changes in the uveoscleral outflow pathway, which may lead to an increa
46 ole for increased MMPs in the enhancement of uveoscleral outflow that occurs after topical treatment
49 ult rabbits, IOP was lower, aqueous flow and uveoscleral outflow were higher, and fluorophotometric o
50 eadings were compared, IOP, aqueous flow and uveoscleral outflow were higher, fluorophotometric outfl
52 subjects in their inability to increase the uveoscleral outflow with increases in aqueous inflow.
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