Prostaglandins (PG) are known to alter regional ocular blood flow and exhibit vasoactive properties in isolated ocular blood vessels. A variety of animal experiments indicate that endogenous PGs play a role in the regulation of retinal (RBF) and choroidal (ChBF) blood flow. There is also evidence that the prostaglandin pathway is involved in the activation of NO production in humans, however, the mechanisms for interactions between PG and NO in ocular vasculature are still unclear.

Animal studies suggest that retinal and choroidal blood flow decrease after administration of indomethacin (a nonspecific cyclooxygenase inhibitor). More recently, it has been shown that indomethacin injected intravenously decreased optic nerve oxygen tension and reduced the CO2 reactivity. This is probably the result of decreased blood flow through vasoconstriction of vessels in the optic nerve. Systemic administration of indomethacin also diminishes cerebral, renal and mesenteric blood flow by an unknown mechanism. However, no clinical trials exist so far investigating the effects of indomethacin on ocular blood flow. Therefore, the aim of this study is to investigate the effect of indomethacin on ocular blood flow in healthy humans.