An objective method for reliably estimating the width of retinal vessels is presented. A computerized microdensitometer scans film negatives of fundus photographs and reconstructs black and white images of the fundus on a visual display terminal. After this initial scan, a desired region of a retinal vessel is selected with moveable cursors, and a cross-sectional density profile through the vessel is plotted. Vessel width is determined by the half-height width of the profile of the minimum (least transmitting) and average background film densities. Measurement sites can be accurately reproduced on different negatives by landmark mapping. A series of ten fundus photographs were taken of three healthy human eyes, and the width of the superior temporal vein was measured in two places on alle negatives. The coefficient of variation of the six sets ranged from 1.2 and 3.4% with an average of 2.2%.
To the Editor.—
Gole and Gannon1 have apparently misconstrued our letter.2 It was not our intention that the proposed model for the development of retinopathy of prematurity (ROP) be accepted as a basis for clinical treatment. Instead, this model was propounded in hopes of stimulating further research into the possible role of CO2 in the pathogenesis of ROP. Therefore, we must respond to their charges of "speculation" by stating that this letter was obviously speculative in nature; however, all the assumptions made can be defended.
Gordon et al1 were the first to note the association of retrolental fibroplasia (RLF) with the administration of high concentrations of oxygen to premature infants. Since that time, clinical research has demonostrated that RLF can develop in a variety of circumstances. Typically, this retinopathy arises after the cessation of supplemental oxygen therapy to neonates. Currently, the most widely accepted paradigm proposes that the neovascularization of RLF is the immature vascular system's response to a retina that has become hypoxic after the withdrawal of supplemental oxygen.
SUMMARY
The neovascular changes of the retinopathy of prematurity can occur in premature infants in three settings: (1) when high levels of supplemental oxygen are administered, neovascularization usually commences shortly after cessation of oxygen therapy; (2) when supplemental oxygen is given for long periods of time, neovascularization can develop while the infant is still receiving oxygen; and (3) neovascularization can occur without exposure to any supplemental oxygen. We propose a model which can explain the occurrence of the retinopathy of prematurity in all these settings.
Our model demonstrates that whenever the retinopathy of prematurity occurs, arterial oxygen levels are inappropriately high in relation to the stage of retinal vessel development, even in premature neonates not given supplemental oxygen. The inhibitory effect of these elevated oxygen tensions upon carbon dioxide removal is indicated as a possible cause of neovascularization by leading to tissue acidosis and vasodilatation.
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