scholarly journals A Study on the Drug Concentration in Fellow Eyes After Unilateral Intravitreal Injection of Conbercept Into New Zealand Rabbit Eyes

2021 ◽  
Vol 12 ◽  
Author(s):  
Yu Di ◽  
Haiyan Xu ◽  
Junjie Ye ◽  
Zijian Guo
Keyword(s):  
New Zealand ◽  
Intravitreal Injection ◽  
Aqueous Humor ◽  
Drug Concentration ◽  
Vitreous Humor ◽  
Vascular Endothelial ◽  
Ocular Diseases ◽  
Experimental Animal Study ◽  
Endothelial Growth Factor ◽  
Fellow Eyes

Intravitreal injections of anti-vascular endothelial growth factor (VEGF) have become increasingly popular in the treatment of ocular diseases. However, few studies have determined the efficiency of unilateral intravitreal anti-VEGF injection in the fellow eye. Herein, we performed a study to investigate the drug concentration in fellow eyes and venous serum after unilateral intravitreal injection of conbercept into rabbit eyes. This is an experimental animal study. Thirty male New Zealand rabbits (60 eyes) were used. One eye of each rabbit was intravitreally injected with 0.5 mg of conbercept. Both eyes from six rabbits were enucleated on days 1, 3, 7, 14, and 30. Conbercept concentrations were measured in the serum, aqueous humor, and vitreous humor. We found conbercept was detected in the fellow eyes and serum of rabbits. Conbercept concentrations in the vitreous humor of the fellow eyes increased from 74.11 ng/ml on day 1 to 246.69 ng/ml on day 3 and then declined to 69.11 ng/ml after 30 days. The concentration in the aqueous humor peaked on day 1 with a concentration of 244.82 ng/ml and declined to 40.13 ng/ml after 30 days. The maximum conbercept concentrations in the aqueous humor and vitreous humor of fellow eyes were similar, which were 0.2 and 1.3% of those of the injected eye, respectively. A peak concentration of 102.49 ng/ml was achieved in the venous serum 1 day after intravitreal injection of conbercept, which was 0.08 and 0.5% of those of the maximum conbercept concentrations in the vitreous humor and aqueous humor of the injected eye, respectively, and 41.5 and 41.8% of the maximum conbercept concentrations in the vitreous humor and aqueous humor of the non-injected eye, respectively. In conclusion, after intravitreal injection of 0.5 mg of conbercept into rabbit eyes, very small amounts of conbercept were detected in the fellow non-injected eyes and venous serum.

scholarly journals Changing of the vascular endothelial growth factor concentration in aqueous humor before and after intravitreal injection of Bevacizumab adjuvant treating complicated proliferative diabetic retinopathy

2021 ◽  
Vol 63 (7) ◽  
pp. 17-21
Author(s):  
Tuan Anh Vu ◽  
◽  
Tuan Thanh Hao Nguyen ◽  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Diabetic Retinopathy ◽  
Growth Factor ◽  
Intravitreal Injection ◽  
Aqueous Humor ◽  
Proliferative Diabetic Retinopathy ◽  
Vascular Endothelial ◽  
Study Results ◽  
Before And After ◽  
Endothelial Growth Factor

This article studies the changing of concentration of vascular endothelial growth factor (VEGF) from the aqueous humor sample, before and after intravitreal injection of Bevacizumab, for treatment of complicated proliferative diabetic retinopathy (PDR) and the correlation with clinical features. This study was implemented with prospective and interventional case series; 1.25 mg of Bevacizumab was injected into the vitreous cavity to treat PDRin 48 eyes of 29 patients. Aqueous humor samples were obtained before intravitreal injection of Bevacizumab and one week after. Study results showed: VEGF concentration decreased from 474.23±361.32 pg/ml to 16.96±18.11 pg/ml (p=0.000) at all eyes after one-week injection. There were no differences in levels of VEGF among groups according to the vitreous haemorrhage, tractional retinal detachment, and retinal fibrosis. Therefore, the study exhibited a better understanding of the role of anti-VEGF in the adjuvant treatment of complicated PDR.

Increased Vascular Endothelial Growth Factor Levels in Aqueous Humor and Serum of Patients with Quiescent Uveitis

2007 ◽  
Vol 17 (6) ◽  
pp. 938-942 ◽  
Author(s):  
M.P. Paroli ◽  
C. Teodori ◽  
M. D'alessandro ◽  
P. Mariani ◽  
G. Iannucci ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Aqueous Humor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals eNOS-induced vascular barrier disruption in retinopathy by c-Src activation and tyrosine phosphorylation of VE-cadherin

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Takeshi Ninchoji ◽  
Dominic T Love ◽  
Ross O Smith ◽  
Marie Hedlund ◽  
Dietmar Vestweber ◽  
...  
Keyword(s):  
No Synthase ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Ocular Diseases ◽  
Oxygen Induced Retinopathy ◽  
No Formation ◽  
Therapy Development ◽  
Endothelial Growth Factor ◽  
Deutsche Forschungsgemeinschaft

Background:Hypoxia and consequent production of vascular endothelial growth factor A (VEGFA) promote blood vessel leakiness and edema in ocular diseases. Anti-VEGFA therapeutics may aggravate hypoxia; therefore, therapy development is needed.Methods:Oxygen-induced retinopathy was used as a model to test the role of nitric oxide (NO) in pathological neovascularization and vessel permeability. Suppression of NO formation was achieved chemically using L-NMMA, or genetically, in endothelial NO synthase serine to alanine (S1176A) mutant mice.Results:Suppression of NO formation resulted in reduced retinal neoangiogenesis. Remaining vascular tufts exhibited reduced vascular leakage through stabilized endothelial adherens junctions, manifested as reduced phosphorylation of vascular endothelial (VE)-cadherin Y685 in a c-Src-dependent manner. Treatment with a single dose of L-NMMA in established retinopathy restored the vascular barrier and prevented leakage.Conclusions:We conclude that NO destabilizes adheren junctions, resulting in vascular hyperpermeability, by converging with the VEGFA/VEGFR2/c-Src/VE-cadherin pathway.Funding:This study was supported by the Swedish Cancer foundation (19 0119 Pj ), the Swedish Research Council (2020-01349), the Knut and Alice Wallenberg foundation (KAW 2020.0057) and a Fondation Leducq Transatlantic Network of Excellence Grant in Neurovascular Disease (17 CVD 03). KAW also supported LCW with a Wallenberg Scholar grant (2015.0275). WCS was supported by Grants R35 HL139945, P01 HL1070205, AHA MERIT Award. DV was supported by grants from the Deutsche Forschungsgemeinschaft, SFB1450, B03, and CRU342, P2.

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