The physiologic mechanism of photocoagulation can been seen in the following steps. The physical light energy is absorbed in the melanin of the retinal pigment epithelium. The adjacent photoreceptors are destroyed and are replaced by a glial scar and the oxygen consumption of the outer retina is reduced. Oxygen that normally diffuses from the choriocapillaris into the retina can now diffuse through the laser scars in the photoreceptor layer without being consumed in the mitochondria of the photoreceptors. This oxygen flux reaches the inner retina to relieve inner retinal hypoxia and raise the oxygen tension. As a result, the retinal arteries constrict and the bloodflow decreases. Hypoxia relief reduces production of growth factors such as VEGF and neovascularization is reduced or stopped. Vasoconstriction increases arteriolar resistance, decreases hydrostatic pressure in capillaries and venules and reduces edema formation according to Starling's law. Vitrectomy also improves retinal oxygenation by allowing oxygen and other nutrients to be transported in water currents in the vitreous cavity from well oxygenated to ischemic areas of the retina. Vitrectomy and retinal photocoagulation both improve retinal oxygenation and both reduce diabetic macular edema and retinal neovascularization.