Hyperbaric oxygen therapy ameliorates the blood–retinal barrier breakdown in diabetic retinopathy

@article{Chang2006HyperbaricOT,
  title={Hyperbaric oxygen therapy ameliorates the blood–retinal barrier breakdown in diabetic retinopathy},
  author={Yun-Hsiang Chang and Po-Liang Chen and Ming‐Cheng Tai and Chiao-Hong Chen and D W Lu and Jiann-Torng Chen},
  journal={Clinical \& Experimental Ophthalmology},
  year={2006},
  volume={34}
}
Background:  To study the effect of hyperbaric oxygen (HBO) therapy on diabetic retinopathy in a streptozotocin‐induced diabetic rat model. 
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30 Citations
Background Citations
7
Methods Citations
2
Results Citations
1

30 Citations

Delayed response of the retina after hyperbaric oxygen exposure
Purpose:  To examine retinal electrophysiological function and retinal thickness in healthy eyes before and after hyperbaric oxygen (HBO) exposure.
Hyperbaric oxygen therapy and the possibility of ocular complications or contraindications
  • C. McMonnies
  • Medicine, Biology
    Clinical & experimental optometry
  • 2015
TLDR
Hyperbaric oxygen therapy increases oxygen pressure and the concentration of reactive oxygen species in blood and tissues to treat diabetic leg ulcers and diabetic retinopathy; however, due to their cytotoxic properties, an excess of reactiveoxygen species in tissues and/or deficiencies in antioxidant activity, may contribute to complications of hyperbaricoxy therapy.
The effects of hyperbaric oxygen therapy on diabetic retinopathy: A preliminary study.
Hypoxia and Dark Adaptation in Diabetic Retinopathy: Interactions, Consequences, and Therapy
TLDR
The use of nocturnal illumination to prevent dark adaptation, specifically reducing the rod photoreceptor dark current, should ameliorate diabetic retinopathy.
The effect of hyperbaric oxygen therapy on retinal thickness and progression of retinopathy in patients with Type 2 diabetes: a prospective cohort study
TLDR
HBOT has both a thinning effect on the choroid layer in all three groups and a thickening effect in the macula in the mild-moderate non-proliferative diabetic eyes.
Atorvastatin: an efficient step forward in mesenchymal stem cell therapy of diabetic retinopathy.
Is There Aggravating Effect of Hyperbaric Oxygen Therapy on Diabetic Retinopathy and Macular Edema?
TLDR
The fact that there was no loss in visual acuity during HBOT but occurred on day after the completion of HBOT and that NVD was developed in this period should be questioned suggests that the sudden drop in oxygen saturation after the end ofHBOT may have contributed to this situation.
The use of hyperbaric oxygen therapy in ophthalmology.
Acute Effect of Hyperbaric Oxygen Therapy on Macular and Choroidal Thickness in Patients with Type 2 Diabetes and Diabetic Foot Ulcers: Optical Coherence Tomography Based Study
Long-term treatment with hyperbaric air improves hyperlipidemia of db/db mice.
TLDR
Exposure of HBA could have beneficial effects on lipid metabolism in patients with type 2 diabetes mellitus, according to the results of this study.
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References

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TLDR
Rats with experimental diabetes (induced by streptozocin [Streptozotocin]) were studied by vitreous fluorophotometry and horseradish peroxidase tracer technique, and three types of retinal pigment epithelial (RPE) lesions were observed.
Vascular endothelial growth factor plays a role in hyperpermeability of diabetic retinal vessels.
TLDR
Findings indicate that vascular endothelial growth factor plays an important role in blood-retinal barrier breakdown in diabetic retinopathy.
Early breakdown of the blood-retinal barrier in diabetes.
TLDR
A new clinical method by vitreous fluorophotometry appears to satisfy the necessary requirements in that it is quantitative and shows good reproducibility and high sensitivity, and revealed the presence of a significant breakdown of the blood-retinal barrier in the early stages of retinal involvement in diabetes.
Immunohistochemical detection of blood-retinal barrier breakdown in streptozotocin-diabetic rat
TLDR
It is suggested that the duration of diabetes has an influence on BRB breakdown and that each substance in the blood starts to permeate the vascular wall individually.
Ocular Lesions in Rats Rendered Chronically Diabetic with Streptozotocin
TLDR
The first results of a long-term study on rats rendered chronically diabetic with streptozotocin are presented and the basement membranes of diabetic animals showed focal thickenings containing basement membranelike and/or fibrillar material with the periodicity of collagen, but an increase of mean basement membrane width was not found compared with the controls.
Origin of the microangiopathic changes in diabetes
TLDR
This article will briefly describe a number of ultrastructural, biochemical and haemostatic processes related to microangiopathy and discuss possible pathogenic interactions which may lead to the development of the pathological lesion.
The role of growth factors in proliferative diabetic retinopathy
TLDR
A mechanism is outlined which takes into account both local and systemic factors in the development of PDR, but clearly systemic factors play a part if nephropathy is truly a second risk factor for PDR.
Retinal leakage in retinal vein occlusion: reduction after hyperbaric oxygen.
TLDR
A 54-year-old woman with a history of bilateral central retinal vein occlusion with cystoid macular edema with possible implications of an inflammatory process developed a hemispheric retinal veins occlusions with cyStoid macULAR edema in her only seeing eye.
The relation between expression of vascular endothelial growth factor and breakdown of the blood-retinal barrier in diabetic rat retinas.
TLDR
It is suggested that VEGF plays a role in the budding of retinal neovascularization and, as a result, could induce proliferative diabetic retinopathy.
Ultrastructural localization of blood-retinal barrier breakdown in diabetic and galactosemic rats.
TLDR
It is suggested that specific sites of BRB compromise are infrequent but that once albumin has crossed the RCE or RPE it freely permeates the retinal tissue by filling intercellular spaces and permeating the membranes of cells not implicated in BRB formation.
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