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1 ries after application of nitroglycerine and brimonidine.
2 e common with BBFC than with brinzolamide or brimonidine.
3 % with brinzolamide, and 20.6% to 31.3% with brimonidine.
4 reater efficacy than concomitant timolol and brimonidine.
5 cular hypertensive retinas was attenuated by brimonidine.
6                       They were treated with brimonidine 0.15% for 8 weeks and designated for retesti
7 BFC (n = 193), brinzolamide 1% (n = 192), or brimonidine 0.2% (n = 175) BID.
8 results and large number of drop-outs in the brimonidine 0.2% arm suggest that more research is neces
9                          Brinzolamide 1% and brimonidine 0.2% fixed combination administered BID had
10                       While randomization to brimonidine 0.2% was protective compared to timolol 0.5%
11 ed to topical treatment with timolol 0.5% or brimonidine 0.2%.
12  and brimonidine, 0.2%; brinzolamide, 1%; or brimonidine, 0.2%) 1 drop 3 times daily for 3 months.
13  and brimonidine, 0.2%; brinzolamide, 1%; or brimonidine, 0.2%, 3 times daily for 3 months.
14 e fixed combination of brinzolamide, 1%, and brimonidine, 0.2%, can safely and effectively lower IOP
15 t fixed combination of brinzolamide, 1%, and brimonidine, 0.2%.
16 ion (fixed-combination brinzolamide, 1%, and brimonidine, 0.2%; brinzolamide, 1%; or brimonidine, 0.2
17 with fixed-combination brinzolamide, 1%, and brimonidine, 0.2%; brinzolamide, 1%; or brimonidine, 0.2
18           Patients were treated with 10 g of brimonidine, 0.33%, gel applied under occlusion for hemo
19                                      Topical brimonidine, 0.33%, gel can result in systemic central n
20                                      Topical brimonidine, 0.33%, gel has been reported for the use of
21 he risk of systemic toxic effects of topical brimonidine, 0.33%, gel when used for hemostasis.
22     Rats were treated intraperitoneally with brimonidine (1 mg/kg) or phosphate-buffered saline (PBS)
23                                        Next, brimonidine (100 ug/kg, IP) was administered either one
24                 After the 8-week course with brimonidine, 14 of the 17 patients who completed the stu
25 brimonidine, 22.9%; brinzolamide, 18.6%; and brimonidine, 17.3%; P = .31), most of which were ocular.
26 eatment-related adverse effect (brinzolamide-brimonidine, 22.9%; brinzolamide, 18.6%; and brimonidine
27 0.19 mmHg; brinzolamide, 25.9 +/- 0.20 mmHg; brimonidine, 26.0 +/- 0.19 mmHg).
28 .37 (2.94; 5.83), timolol 3.70 (3.16; 4.24), brimonidine 3.59 (2.89; 4.29), carteolol 3.44 (2.42; 4.4
29 by the antiglaucoma drugs dipivefrine (72%), brimonidine (70%), and carbachol (78%).
30                                              Brimonidine, a selective alpha(2)-adrenoceptor agonist,
31                                              Brimonidine administration initiated 10 days after IOP e
32 nd CBSM cells indicates the possibility that brimonidine affects uveoscleral outflow.
33 -lowering effect than either brinzolamide or brimonidine alone and displayed a safety profile consist
34 the present study, we examined the effect of brimonidine (alpha(2)-adrenoceptor agonist) on RGC survi
35        Other alpha(2)-adrenoceptor agonists, brimonidine and apraclonidine, acted in a similar way to
36 2+ mobilization in the Pe in response to the brimonidine and carbachol combination was either blocked
37                    The suppressive action of brimonidine and medetomidine was completely blocked by c
38 ion of synaptic transmission at IPL and that brimonidine and other alpha2 agonists may protect RGCs u
39 lso suppressed in a dose-dependent manner by brimonidine and other alpha2 receptor agonists, such as
40  initial drug of choice, but latanoprost and brimonidine are now being recommended by many as alterna
41                     However, latanoprost and brimonidine are often given as monotherapy as well as ea
42 he beneficial effect of randomization to the brimonidine arm was independent of possible differences
43 , therefore, urge against the use of topical brimonidine as a hemostatic agent until its safety is fu
44 ted using poly(lactic acid) (PLA) to release brimonidine at a constant rate for 35 days and microneed
45  There is high-quality evidence that topical brimonidine, azelaic acid, and ivermectin, as well as or
46                                              Brimonidine, but not timolol, showed significant protect
47 not possible to define a quantity with which brimonidine can be used safely, nor can a safe wound siz
48 rostone concomitant therapy, and timolol and brimonidine concomitant therapy.
49                  Concomitant latanoprost and brimonidine demonstrated better efficacy than the dorzol
50 icantly affect tissue permeability at either brimonidine dose.
51 t of rabbits receiving twice daily, standard brimonidine drops.
52 erase (PDE4) inhibitor, indicating that this brimonidine effect is mediated by the alpha2 receptor th
53  carbachol, the alpha 2-adrenoceptor agonist brimonidine elicited large Ca2+ increases (> 10-fold) in
54 ministration of a glaucoma medication (i.e., brimonidine) formulated for sustained release in the sup
55                          In vitro release of brimonidine from the GMS drops and gel properties were q
56  IOP reduction in rabbits receiving a single brimonidine GMS drop was comparable to that of rabbits r
57 t 3 months, the mean IOP of the brinzolamide-brimonidine group (16.3-19.8 mm Hg) was significantly lo
58 e group (19.3-20.9 mm Hg; P </= .002) or the brimonidine group (17.9-22.5 mm Hg; P < .001) across all
59 nt study was that patients randomized to the brimonidine group were statistically less likely to have
60                          This indicates that brimonidine has a neuroprotective activity unrelated to
61                     alpha2 Agonists, such as brimonidine, have been shown to protect retinal ganglion
62 onidine was introduced for this use in 1966, brimonidine in 1974, and apraclonidine in 1978.
63                        The transport of [3H]-brimonidine in bovine RPE-choroid explants was evaluated
64     A carrier-mediated transport process for brimonidine in RPE was demonstrated in bovine RPE-choroi
65 l ganglion cells by alpha2 agonists, such as brimonidine, in animal models of glaucoma and retinal is
66                                              Brimonidine increased C by 0.005 +/- 0.0005 muL/min/mm H
67                                              Brimonidine increased pro-MMP-9 an average of 116% +/- 3
68  determine how the alpha2-adrenergic agonist brimonidine influences loss of Thy1 promoter activation.
69                             The transport of brimonidine into (choroid-to-retina transport [inward])
70 gnificant role in modulating the movement of brimonidine into and out of the eye.
71                                   Currently, brimonidine is classified as a category B medication wit
72 file and risk of systemic toxic effects when brimonidine is used topically for hemostasis is unknown.
73                                     A single brimonidine-loaded GMS drop was administered to 5 normot
74 t time, that the highly-targeted delivery of brimonidine-loaded microspheres into the supraciliary sp
75                     To test this hypothesis, brimonidine-loaded microspheres were formulated using po
76 fference: -1.4 mmHg; P < 0.0001; t test) and brimonidine (LS mean difference: -1.5 mmHg; P < 0.0001).
77 ce, 0.035; 95% CI, 0.008-0.061; P = .02) and brimonidine (mean difference, -0.015; 95% CI, -0.082 to
78 l progressed faster than those randomized to brimonidine (mean rates of progression, -0.38 +/- 0.9 vs
79 ctivity compared with either brinzolamide or brimonidine monotherapy while providing a safety profile
80                                          The brimonidine neuroprotective effect was abolished by an a
81                                              Brimonidine or NMDA receptor blockers protected RGCs in
82 cant changes in elevated IOP was found after brimonidine or PBS treatment when compared with the nont
83                   Systemic administration of brimonidine or timolol caused little decrease in IOP.
84                      Systemic application of brimonidine or timolol had little effect on IOP.
85                                              Brimonidine or timolol was administered, either at the t
86 he control with elevated IOP but without any brimonidine/PBS treatment.
87                                              Brimonidine pretreatment also significantly reduced NMDA
88 dence suggests that alpha2 agonists, such as brimonidine, protect retinal ganglion cells (RGCs) from
89                                         This brimonidine protection is also enhanced significantly by
90                                              Brimonidine protects RGCs in the rabbit excitotoxicity m
91                                              Brimonidine reduced the progressive loss of ganglion cel
92 ed with progression whereas randomization to brimonidine revealed a protective effect (HR = 0.26, 95%
93                                              Brimonidine significantly improved impaired retinal vasc
94                                              Brimonidine significantly protected RGCs from elevated I
95                            Pretreatment with brimonidine significantly reduced NMDA-elicited currents
96 ratories Inc., Fort Worth, TX], brinzolamide/brimonidine [Simbrinza; Alcon Laboratories Inc.], and la
97                    Rate analysis showed that brimonidine slowed the initial rate of fluorescent cell
98 5 different human donors received control or brimonidine tartrate (45 nM) for 1, 3, or 7 days.
99 rochloride, apraclonidine hydrochloride, and brimonidine tartrate constitute the three topical alpha
100 eight healthy subjects was treated with 0.2% brimonidine tartrate ophthalmic solution to induce pupil
101 e advantages, but triple-therapy dorzolamide/brimonidine/timolol (dorz/brim/tim) is only available in
102                      Both inward and outward brimonidine transport decreased at 5 microM compared wit
103  amount of cell death gradually increased in brimonidine-treated animals.
104  stimulus intensity was compared between the brimonidine-treated, miotic eye and the untreated eye.
105 one brimonidine treatment, and 55+/-6% after brimonidine treatment every other day (P<0.05 for both b
106     Almost all RGCs were protected following brimonidine treatment for 3 weeks both in groups A and B
107 e treatment every other day (P<0.05 for both brimonidine treatment groups compared to the control gro
108                                              BRIMONIDINE TREATMENT PRODUCED SIGNIFICANT REDUCTION IN
109  baseline in control mice, 51+/-6% after one brimonidine treatment, and 55+/-6% after brimonidine tre
110  RGCs, these findings indicate that repeated brimonidine treatments may protect RGC health following
111                                     Repeated brimonidine treatments protect against loss of fluoresce
112  neurons in the group that received repeated brimonidine treatments was greater than the control grou
113 cts on the fellow untreated eye, compared to brimonidine twice-daily eye drops.
114 NPE, 10 microM acetylcholine (ACh), 1 microM brimonidine (UK 14304), or 1 microM epinephrine each eli
115 laucoma patients not previously treated with brimonidine underwent retinal vascular autoregulation te
116 l (representing choroid-to-retina transport) brimonidine uptake in ARPE-19 cells showed temperature d
117                                  Basolateral brimonidine uptake increased by 35% at extracellular pH
118                   This suppressive action of brimonidine was blocked by alpha2 antagonists, cAMP anal
119                            The uptake of [3H]brimonidine was evaluated in differentiated ARPE-19 cell
120                   This suppressive effect of brimonidine was substantially enhanced by background add
121 y lower with brinzolamide than with BBFC and brimonidine, whereas blurred vision and ocular discomfor

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