Role of Nitric Oxide in Regulation of Retinal Blood Flow in Response to Hyperoxia in Cats

Abstract

To investigate whether nitric oxide (NO) regulates retinal circulation during and after induction of hyperoxia in cats. Hyperoxia was induced for 10 minutes with 100% oxygen. The vessel diameter and blood velocity were measured simultaneously in second-order retinal arterioles by laser Doppler velocimetry; the retinal blood flow (RBF) and wall shear rate (WSR) were calculated during and after hyperoxia. PBS, L-NAME, D-NAME, BQ-123, BQ-788, and 7-nitroindazole (7-NI) were administered before induction of hyperoxia. In the PBS group, vessel diameter, blood velocity, and RBF decreased during hyperoxia and returned to baseline within 10 minutes after hyperoxia ended. WSR decreased transiently and then returned to baseline by the delayed constriction of retinal arterioles during hyperoxia. In the l-NAME and BQ-788 groups, the decreases in RBF during hyperoxia did not differ from those in the PBS group. However, the recovery of RBF after hyperoxia ended was attenuated significantly until 20 minutes after hyperoxia ended in both groups compared with the PBS group (P < 0.05). In the BQ-123 group, the intravitreous injection of BQ-123 caused less reduction of blood velocity and RBF during hyperoxia compared with that in the PBS group, whereas the RBF immediately returned to baseline after hyperoxia. D-NAME and 7-NI did not affect RBF in response to hyperoxia. The current results indicate that NO contributes to RBF recovery after hyperoxia, probably through the action of endothelial NOS via the ETB receptor in the vascular endothelium of the retinal arterioles, suggesting that the RBF response to hyperoxia may be used to evaluate the endothelial function of the retinal arterioles.