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Updated: Apr 20, 2026

Quantification of Vascular Parameters in Whole Mount Retinas of Mice with Non-Proliferative and Proliferative Retinopathies
Published on: March 12, 2022
Quantitative assessment of the human retinal microvasculature with or without vascular comorbidity
Priscilla E Z Tan1, Paula K Yu1, Stephen J Cringle1
1Centre for Ophthalmology and Visual Science, University of Western Australia, Perth, Australia Lions Eye Institute, University of Western Australia, Perth, Australia.
Insights
Cardiovascular comorbidities may alter retinal capillary density, even before ocular disease is evident. These microvascular changes in the retina could impact neuronal function and disease mechanisms.
Area of Science:
- Ophthalmology
- Cardiology
- Microvascular Research
Background:
- Cardiovascular comorbidities are a leading cause of morbidity and mortality.
- The relationship between systemic vascular health and retinal microvasculature, particularly before overt ocular disease, requires further investigation.
Purpose of the Study:
- To investigate if cardiovascular comorbidities are associated with quantitative changes in the retinal microvasculature in individuals without known ocular disease.
- To explore potential links between systemic vascular disease and early-stage retinal vascular alterations.
Main Methods:
- Comparison of retinal microvasculature in donors with cardiovascular comorbidities (diseased group) versus those without vascular disease (control group).
- Utilized perfusion fixation, endothelial f-actin labeling, and confocal scanning laser microscopy for high-resolution imaging.
- Quantified capillary diameter and density, and identified pathological vascular changes using 2D and 3D reconstructions.
Main Results:
- Significant differences in capillary densities were observed across different retinal layers in the diseased group.
- A notable decrease in capillary density was found in the nerve fiber and retinal ganglion cell layers of the diseased group compared to controls.
- Pathological vascular changes, including microaneurysms and tortuous venules, were identified in the diseased group.
Conclusions:
- Cardiovascular comorbidities may induce changes in human retinal capillary density prior to the clinical manifestation of ocular diseases.
- These microvascular density alterations may correlate with neuronal function and provide insights into pathogenic mechanisms of retinal vascular disease.
Purpose:
To determine whether morbidity and mortality in patients with cardiovascular comorbidities, but no known ocular disease, is related to demonstrable quantitative changes in the retinal microvasculature.
Methods:
Eleven eyes from 8 donors with cardiovascular comorbidities as a diseased group were compared with 16 eyes from 14 donors free from vascular disease as a control group. All eyes had no known ocular disease. The retina was perfusion-fixed and labeled for endothelial f-actin using micro-cannulation techniques. The retinal microvasculature 3 mm superior to the optic disc was imaged with confocal scanning laser microscopy. Quantitative measurements of capillary diameter and density were obtained using two-dimensional image reconstructions. Pathological vascular changes in other regions of the retinal vasculature found in the diseased group were identified and reconstructed in two or three dimensions.
Results:
Capillary densities were significantly different between each capillary network in the diseased group. There was a significant decrease in density between both the nerve fiber layer and retinal ganglion cell layer of the diseased group when compared with those layers in the control eyes. There were pathological vascular changes including microaneurysms and tortuous, dilated venules identified in the diseased group.
Conclusions:
Cardiovascular comorbidities may be associated with changes to the capillary density within the human retinal microvasculature, before the manifestation of known ocular diseases. These differences in capillary density may have important correlations with neuronal function and facilitates the basis of understanding pathogenic mechanisms in retinal vascular disease.

