Abstract
Purpose: :
To investigate whether nitric oxide (NO) contributes to regulation of retinal circulation during and after induction of hyperoxia in cats.
Methods: :
NG-nitro-L-arginine-methylester (L-NAME; n=6), a NO synthase (NOS) inhibitor; NG-nitro-D-arginine-methylester (D-NAME; n=7), an inactive isomer; BQ-123 (n=7), an endothelin (ET) A receptor antagonist; BQ-788 (n=6), an ETB receptor antagonist; or phosphate-buffered saline (PBS; n=7) was injected intravitreously into feline eyes. A selective neuronal NOS inhibitor, 7-nitroindazole (7-NI; n=7), was injected intraperitoneally. Hyperoxia was induced for 10 minutes by inhalation of 100% oxygen. We measured the vessel diameter and blood velocity simultaneously in large retinal arterioles in cats by laser Doppler velocimetry and the retinal blood flow (RBF) was calculated during and after hyperoxia.
Results: :
In the PBS group, the vessel diameter (-18.3%±2.1%, P<0.05), blood velocity (-23.4%±3.3%, P<0.05), and RBF (-48.4%±2.6%, P<0.05) decreased during hyperoxia. These parameters increased and recovered to baseline within 10 minutes after cessation of hyperoxia. In the L-NAME and BQ-788 groups, no changes occurred in RBF during hyperoxia compared with the PBS group. However, RBF recovery after cessation of hyperoxia was attenuated significantly until 20 minutes after cessation of hyperoxia in both groups compared with the PBS group (P<0.05). In the BQ-123 group, the decreased RBF during hyperoxia was significant (P<0.05) compared with the PBS group, whereas the RBF returned to baseline over the same time course as the PBS group. 7-NI did not affect changes in RBF in response to hyperoxia.
Conclusions: :
NO contributes to RBF recovery after hyperoxia. Further, the NO synthesized by the action of endothelial NOS via the ETB receptor in the retinal endothelium may regulate RBF after hyperoxia. These findings suggest that the RBF response to hyperoxia may be used to evaluate the endothelial function of the retinal arterioles.