A self-portrait of Sir Stewart Duke-Elder.
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Biomedical subjects
Publications and source records attributed to M C Colenbrander.
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In diabetic retinopathy, a low resistance of flow between choroid and retina is found which goes with an increased intake of tissue fluid into the retinal vessels and the appearance of retinal oedema. Light coagulation destroys the choriocapillaris which does not regenerate. As less fluid becomes available to be sucked up by the retinal vessels, the oedema will now disappear and consequently, the retinopathy subsides.
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In the eye all membranes are more or less under tension, as elsewhere in the body. Hence the hydrostatic pressure in the choroid is less than in the retina. The available pressure difference within the bloodvessels would be less for the retina than for the choroid, if the arteries to the retina did not have a much larger bore than those to the choroid. Hence the bloodstream for the retina is slower and fluorescein appears later in the retina than in the choroid. There is a flow of tissue fluid from the choroid to the retina. It is absorbed by the retinal vessels. The larger the flow, the larger are the retinal veins, till retinal oedema occurs. Then the tissue pressure within the retina rises sharply and the capillaries become strangulated. But a few capillaries remain open and are blown up to arterio-venular shunts. Micro-aneurysmata arise as abortive vessel sprouts. It is plausible that lightcoagulation sticks the lamellae of Bruch's membrane together, to the extent that the development of oedema is arrested.