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Abstract
A frequently cited theory for the pathogenesis of neovascularization in diabetic retinopathy is that retinal hypoxia and/or ischemia release a factor which stimulates neovascularization. To the authors' knowledge, there is no direct in vivo evidence in the human proving this theory. One hundred and twenty-two diabetic subjects were studied to see whether worsening retinopathy was associated with changes in conjunctival oxygen tension (pO2). Diabetics without retinopathy had a conjunctival pO2 which was similar to an age-matched normal population. Diabetics with only background retinopathy had a significantly lower conjunctival pO2 than those without retinopathy (P less than 0.01). Diabetics with proliferative retinopathy showed a conjunctival pO2 that was significantly lower than either of the first two groups (P less than 0.05). The lowest value of all was found in patients with rubeosis iridis. Duration of diabetes alone did not correlate significantly to conjunctival pO2. These findings support the hypoxic theory of diabetic neovascular retinopathy.