Age related macula degeneration is one of the most common sight threatening diseases of the elderly. The so called wet form of AMD is caused by choroidal neovascularisation (CNV) of pathological vessels, which lead to leakage, bleeding and macular edema. Several lines of evidence suggest that vascular endothelial growth factor (VEGF) plays a key role in the induction CNV. Recent evidence indicates that overexpression of VEGF in the retinal pigment epithelium may lead to the development of CNV in experimental models, and intravitreal injection of a VEGF blocker prevents the development of experimental CNV. This hypothesis is also supported by the promising effects of anti-VEGF treatment in patients with choroidal neovascularisation. The substances currently in clinical use include ranibizumab (Lucentis®), bevacizumab (Avastin®) and pegaptanib (Macugen®).

However, from a physiological point of view, VEGF also serves as a survival factor for existing vessels and for neuronal cells. Moreover, it has been reported that VEGF induces vasodilatation, most probably by an increased production of nitric oxide. Accordingly one may hypothesize that anti-VEGF treatment is associated with ocular vasoconstriction with unknown long term results. Thus, in the current study, the investigators set out to investigate whether the ocular perfusion is affected by a single intravitreal anti-VEGF.

Inclusion Criteria:

• 40 subjects ≥ 50 years of age
• Subjects with all angiographic subtypes of neovascular wet AMD, already scheduled for intravitreal anti-VEGF therapy in one eye
• Good central or eccentric fixation

Exclusion Criteria:

• History or previous Anti-VEGF therapy
• History or previous intravitreal injection with any drug
• Intraocular pressure ≥ 25
• Glaucoma
• History or presence of thromboembolic events
• Diabetes mellitus
• Blood donation during the previous 3 weeks
• Ametropy ≥ 6 dpt