Abstract
Purpose :
Disturbances in retinal blood flow are involved in the pathophysiology of the most common vision threatening diseases, but the mechanisms underlying these disturbances are unknown. Previous in vitro studies have shown that A2A adrenoceptor agonists induce retinal vasodilatation, but it is unknown whether these results are reproducible in vivo and whether A2A adrenoceptor agonists are involved in vasodilatation during changes in retinal metabolism.
The purpose was to study whether stimulation of A2A adrenoceptors affect flickering light and hypoxia-induced relaxation of retinal vessels in normal persons.
Methods :
Twenty normal persons aged 22-31 were examined in an open controlled interventional study. A dynamic vessel analyser was used to study the diameter of retinal vessels during rest and stimulation with flickering light as a measure of metabolic autoregulation, before and after administration of the A2A adrenoceptor agonist regadenoson (A2A). The examinations were repeated on a second trial day during systemic hypoxia induced by inhalation of a gas mixture of 12.5 % oxygen and 87.5 % nitrogen.
Results :
Hypoxia induced dilatation of retinal arterioles at baseline (p=0.0008) which persisted during simultaneous A2A administration (p=0.02), but was absent during A2A administration alone (p=0.24).
Flicker-induced dilatation of retinal arterioles was significantly reduced after A2A administration both alone (p=0.02), and simultaneously with hypoxia (p<0.0001), as well as during hypoxia alone (p=0.0009).
Conclusions :
A2A adrenoceptor stimulation and hypoxia both reduce flicker-induced dilatation of retinal arterioles. Further investigations should elucidate whether these effects are mediated by the same pathway.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.