Is endothelin-1 action via endothelin receptors a primary mechanism modulating retinal circulatory response to hyperoxia?
These results demonstrate that the enhancement of ET-1 action, possibly caused by the activation of ECE, plays a primary role in regulating the retinal hemodynamic response to hyperoxia.
The results imply that mast cell activation could be involved in the initiation of AP and the early phase of AP-induced MODS. Mechanisms seem to be complex and are still to be elucidated.