Attenuation of Choroidal Neovascularization by β<sub>2</sub>-Adrenoreceptor Antagonism

Lavine, Jeremy A.; Sang, Yanzhi; Wang, Shoujian; Ip, Michael S.; Sheibani, Nader

doi:10.1001/jamaophthalmol.2013.1476

Cited by 44 publications

(54 citation statements)

References 52 publications

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“…This dose in the mouse eyes resulted in significant attenuation of neovascular outgrowth in the laser-induced CNV model. These results suggested that IVP, similar to its systemic administration, 11,14 FIGURE 2. Representative histologic sections of neurosensory retinas in groups I to IV: (A1) group I, (B1) group II, (C1) group III, and (D1) group IV (hematoxylin-eosin stain, magnification: 3400).…”

Section: Discussionmentioning

confidence: 88%

“…15 Most interestingly, the basal level of VEGF is not affected by the b2-AR blockade, since basal VEGF expression and/or activity is essential for a number of systemic functions and neuronal integrity of the retina. 14 Thus, the use of b2-AR blockade may provide a specific mechanism to selectively reduce pathologic levels of VEGF without affecting the basal levels needed for normal tissue functions. Here we also observed an increase in the level of TSP1 in retinas with 0.3 lg propranolol, without a dramatic effect on the levels of VEGF.…”

Section: Discussionmentioning

confidence: 99%

“…12,13 In addition, a few studies 11,14 have demonstrated that systemic prescription of propranolol has antiangiogenic effects and could inhibit retinal and choroidal neovascularization in animal models. To increase ocular local delivery of propranolol and reduce its potential systemic toxicity, the present study was conducted to determine the safe dose of intravitreal propranolol (IVP) in rabbits and mice, and to assess its inhibitory effect in a mouse model of laser-induced CNV.…”

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confidence: 99%

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Ocular Safety of Intravitreal Propranolol and Its Efficacy in Attenuation of Choroidal Neovascularization

Nourinia

Kanavi

Kaharkaboudi

et al. 2015

Invest. Ophthalmol. Vis. Sci.

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Citation: Nourinia R, Rezaei Kanavi M, Kaharkaboudi A, et al. Ocular safety of intravitreal propranolol and its efficacy in attenuation of choroidal neovascularization. Invest Ophthalmol Vis Sci. 2015;56:8228-8235. DOI:10.1167/iovs.15-17169 PURPOSE. Determine the safe dose of intravitreal propranolol (IVP), and evaluate its inhibitory effect on laser-induced choroidal neovascularization (CNV). METHODS.To determine the IVP safe dose, 32 rabbits were divided into 4 groups. Three of these groups received IVP (15 lL) corresponding to 15 lg (group B), 30 lg (group C), and 60 lg (group D). The control group (A) received 15 lL saline. Safety was assessed by ocular examination, electroretinography (ERG), routine histopathologic evaluation, immunohistochemistry for glial fibrillary acidic protein (GFAP), and real-time qPCR for GFAP, VEGF, thrombospondin 1 (TSP1), and pigment epithelium-derived factor (PEDF). A similar experiment was performed in 24 mice by using a 100-fold lower amount of propranolol (0.15, 0.3, and 0.6 lg in 2 lL) based on vitreous volume. For assessment of the angioinhibitory effects of IVP, CNV was induced in 42 mice via laser burns. Mice were divided into two groups: group 1 received the safe dose of IVP (0.3 lg in 2 lL) and group 2 received saline. Neovascularization area was quantified by intercellular adhesion molecule (ICAM)-2 immunostaining of choroidal-scleral flat mounts by using ImageJ software.RESULTS. According to clinical, ERG, and histopathologic findings, 30 lg IVP was chosen as the safe dose in rabbit eyes, comparable to 0.3 lg IVP in mouse eyes. As compared to the control eyes, the development of CNV was attenuated (4.8-fold) in mice receiving 0.3 lg IVP.CONCLUSIONS. Intravitreal propranolol injection up to the final dose of 30 lg in rabbits and 0.3 lg in mice was safe, and was effective in attenuation of CNV in mice.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Ocular Safety of Intravitreal Propranolol and Its Efficacy in Attenuation of Choroidal Neovascularization

Nourinia

Kanavi

Kaharkaboudi

et al. 2015

Invest. Ophthalmol. Vis. Sci.

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“…Furthermore, β-adrenergic blockade has been shown to specifically attenuate choroidal neovascularization and reduce VEGF expression. 26 One retrospective case series reported that patients with neovascular AMD taking systemic β-adrenergic blocking agents were statistically more likely to receive fewer intravitreous injections of bevacizumab than their counter- ence in the rate of β-blocker use between matched patients with exudative and nonexudative AMD. The authors concluded that systemic β-blockers are not protective against choroidal neovascularization, possibly due to the lower administered dosage compared with animal models.…”

Section: Discussionmentioning

confidence: 99%

Topical Dorzolamide-Timolol With Intravitreous Anti–Vascular Endothelial Growth Factor for Neovascular Age-Related Macular Degeneration

et al. 2016

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IMPORTANCE There is a subset of eyes with neovascular age-related macular degeneration (AMD) that have persistent exudation despite fixed-interval intravitreous anti-vascular endothelial growth factor (VEGF) injections.OBJECTIVE To evaluate the effect of topical dorzolamide hydrochloride-timolol maleate on anatomic and functional outcomes in eyes with neovascular AMD and incomplete response to anti-VEGF therapy.DESIGN, SETTING, AND PARTICIPANTS An exploratory, prospective single-arm interventional study at a tertiary referral academic private practice. Patients with neovascular AMD and persistent macular edema despite fixed-interval intravitreous anti-VEGF therapy were enrolled. Baseline spectral-domain optical coherence tomography and clinical data, including visual acuity and intraocular pressure, were obtained at enrollment and from one visit before enrollment. The study was performed at the Retina Service of Wills Eye Hospital and the offices of Mid Atlantic Retina from February 1, 2015, through September 30, 2015. Patients were followed up for at least 2 visits after enrollment. Central subfield thickness, maximum subretinal fluid height, and maximum pigment epithelial detachment height from spectral-domain optical coherence tomography were recorded at each visit.INTERVENTIONS Enrolled eyes received a regimen of topical dorzolamide-timolol twice daily and continued to receive the same intravitreous anti-VEGF therapy at the same interval as received before enrollment for the duration of the study. MAIN OUTCOMES AND MEASURESChange in central subfield thickness was the primary outcome measure. Changes in maximum subretinal fluid height, maximum pigment epithelial detachment height, and visual acuity were the secondary outcome measures. RESULTSTen patients (10 eyes) completed the study. The mean age of the patients was 78.2 years (age range, 65-91 years), and 6 were male. Eight eyes received intravitreous aflibercept, and 2 eyes received intravitreous ranibizumab. All study eyes had been receiving long-term anti-VEGF therapy with the same medication before study enrollment for a mean of 21.9injections. The mean central subfield thickness decreased from 419.7 μm at enrollment to 334.1 μm at the final visit (P = .01). The mean maximum subretinal fluid height decreased from 126.6 μm at enrollment to 49.5 μm at the final visit (P = .02). The mean maximum pigment epithelial detachment height decreased from 277.4 μm at enrollment to 239.9 μm at the final visit (P = .12). The mean logMAR visual acuity were 0.54 at enrollment and 0.48 at the final visit (P = .60). CONCLUSIONS AND RELEVANCEThese data suggest that topical dorzolamide-timolol may reduce central subfield thickness and subretinal fluid in eyes with persistent exudation despite consistent, fixed-interval intravitreous anti-VEGF treatment for neovascular AMD.

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“…10 Recently, the effect of propranolol on diabetic retinopathy, retinopathy of prematurity, and choroidal NV has been studied. [11][12][13] The brilliant success in the treatment of IH with propranolol showed us the idea of using propranolol in corneal NV. To the best of our knowledge, the inhibitory effect of propranolol on corneal NV has not yet been studied.…”

Section: Introductionmentioning

confidence: 99%

The Effect of β Receptor Blockade Through Propranolol on Corneal Neovascularization

Simavlı

Erdurmuş²,

Terzi³

et al. 2014

Journal of Ocular Pharmacology and Therapeutics

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Attenuation of Choroidal Neovascularization by β₂-Adrenoreceptor Antagonism

Cited by 44 publications

References 52 publications

Ocular Safety of Intravitreal Propranolol and Its Efficacy in Attenuation of Choroidal Neovascularization

Ocular Safety of Intravitreal Propranolol and Its Efficacy in Attenuation of Choroidal Neovascularization

Topical Dorzolamide-Timolol With Intravitreous Anti–Vascular Endothelial Growth Factor for Neovascular Age-Related Macular Degeneration

The Effect of β Receptor Blockade Through Propranolol on Corneal Neovascularization

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Attenuation of Choroidal Neovascularization by β2-Adrenoreceptor Antagonism

Cited by 44 publications

References 52 publications

Ocular Safety of Intravitreal Propranolol and Its Efficacy in Attenuation of Choroidal Neovascularization

Ocular Safety of Intravitreal Propranolol and Its Efficacy in Attenuation of Choroidal Neovascularization

Topical Dorzolamide-Timolol With Intravitreous Anti–Vascular Endothelial Growth Factor for Neovascular Age-Related Macular Degeneration

The Effect of β Receptor Blockade Through Propranolol on Corneal Neovascularization

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Attenuation of Choroidal Neovascularization by β₂-Adrenoreceptor Antagonism