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Published on: April 2, 2021
Rod photoreceptor function predicts blood vessel abnormality in retinopathy of prematurity
James D Akula1, Ronald M Hansen, M Elena Martinez-Perez
1Department of Ophthalmology, Children's Hospital Boston and Harvard Medical School, Boston, Massachusetts 02115, USA.
Insights
Early rod dysfunction in retinopathy of prematurity (ROP) models predicts abnormal blood vessel development. This suggests that rod photoreceptors may initiate the vascular changes characteristic of ROP.
Area of Science:
- Ophthalmology
- Developmental Biology
- Physiology
Background:
- Retinopathy of prematurity (ROP) is a leading cause of blindness in premature infants.
- The vascular abnormalities in ROP are a major determinant of visual outcome.
- The underlying mechanisms driving ROP vascular pathology remain incompletely understood.
Purpose of the Study:
- To investigate the hypothesis that early rod photoreceptor dysfunction precedes and predicts the development of ROP-associated vascular abnormalities.
- To determine if rod sensitivity at an early stage (postnatal day 20) can predict later vascular changes.
Main Methods:
- Two rat models of ROP were utilized: a 50%/10% oxygen model and a 75% oxygen model.
- Electroretinography (ERG) was used to assess rod sensitivity (a-wave amplitude).
- Digital fundus imaging and Retinal Image multi-Scale Analysis (RISA) software quantified arteriolar integrated curvature.
Main Results:
- Both ROP models exhibited reduced rod sensitivity and increased arteriolar curvature at postnatal day 20.
- Early low rod sensitivity at postnatal day 20 was a significant predictor of abnormal retinal vasculature at later time points (postnatal days 30 and 60).
- Vascular curvature at postnatal day 20 did not predict subsequent rod sensitivity.
Conclusions:
- Rod photoreceptors may play a causative role in initiating the vascular pathologies observed in retinopathy of prematurity.
- Early detection of rod dysfunction could offer a potential biomarker for predicting ROP severity.
Purpose:
To test the hypothesis that early rod dysfunction predicts the blood vessel abnormalities that are the clinical hallmark of retinopathy of prematurity (ROP).
Methods:
Two rat models of ROP, induced by exposure to alternating 50%/10% oxygen (50/10 model) from postnatal day (P) 0 to P14, or exposure to 75% oxygen (75 model) from P7 to P14, and controls reared in room air were studied. In a longitudinal design, electroretinographic (ERG) records and digital fundus images were obtained at P20 +/- 1, P30 +/- 1, and P60 +/- 1. Rod sensitivity was derived from the ERG a-wave. Integrated curvature for the arterioles was calculated using Retinal Image multi-Scale Analysis (RISA) software.
Results:
In both ROP models, rod sensitivity was low at P20. Sensitivity improved by P60 in the 50/10 model, but remained low in the 75 model. Integrated curvature was high at P20 in both ROP models, decreased nearly to normal by P30 in the 50/10 model, but remained high in the 75 model, even at P60. At P20, rod sensitivity correlated with integrated vessel curvature. Furthermore, low rod sensitivity at P20 predicted abnormal retinal vasculature--that is, high integrated curvature--at P30 and P60. In contrast, vessel curvature at P20 did not predict sensitivity at P30 or P60.
Conclusions:
The rods may instigate the vascular abnormalities that are the clinical hallmark of ROP.
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