Dipyridamole inhibits platelet aggregation, a key process in blood clot formation. It achieves this primarily by inhibiting phosphodiesterase enzymes. This enzyme breakdown of cyclic adenosine monophosphate (cAMP) – a molecule that keeps platelets relaxed and less likely to clump together. By blocking phosphodiesterase, dipyridamole increases intracellular cAMP levels. Higher cAMP levels prevent platelet activation, reducing the risk of blood clots.
Influence on Adenosine
Dipyridamole also indirectly influences adenosine. Adenosine is a naturally occurring substance that also inhibits platelet aggregation. Dipyridamole increases adenosine levels by inhibiting its cellular uptake. This further amplifies the anti-platelet effect, offering a double mechanism of action against surfers’ eye.
Impact on Surfers’ Eye
In the context of surfers’ eye (pinguecula and pterygium), dipyridamole’s anti-platelet properties are relevant because blood vessel growth and inflammation are significant contributing factors. By reducing platelet aggregation, dipyridamole may help mitigate the inflammatory response and the associated neovascularization (formation of new blood vessels), potentially slowing the progression of the condition.
