Abstract

The late Professor I. C. Michaelson's pioneer contributions to the development and pathophysiology of the retinal vasculature have laid the groundwork for a generation of ophthalmic research scientists to pursue this exciting field of investigation. In more recent studies it has been found that, in diabetic retinopathy, branch vein occlusion, sickle cell retinopathy, and retrolental fibroplasia, retinal neovascularisation follows the development of retinal capillary closure. The capillary closure or nonperfusion has been demonstrated by fluorescein angiography. A working hypothesis to explain the clinical and experimental observations is that these areas of nonperfused retina are ischaemic or hypoxic and liberate a theoretical angiogenic or vasoproliferative substance which stimulates the development of retinal neovascularisation. In postulating this working hypothesis it is important to recognise, firstly, that this hypothesis remains to be proved, and, secondly, that retinal neovascularisation may develop from other stimuli such as intraocular inflammation where retinal ischaemia is not apparent.