The effect of nitric oxide on retinal blood flow during hypoxia in cats

To investigate how nitric oxide (NO) contributes to the regulation of retinal circulation during rest and hypoxia in cats.

N(G)-nitro-L-arginine-methyl ester (L-NAME; n = 7), an NO synthase inhibitor; N(G)-nitro-D-arginine methyl ester (D-NAME; n = 6), the inactive isomer; or phosphate-buffered saline (PBS; n = 7) was injected intravitreously. Hypoxia was induced in the cats by the administration of 10% oxygen. Vessel diameter and blood velocity were measured simultaneously in the anesthetized cats with a laser Doppler velocimetry system, and the retinal blood flow (RBF) and wall shear rate (WSR) were calculated as an index of shear stress on the retinal vessel wall.

After intravitreous injection of L-NAME, the vessel diameter (-8.1% +/- 2.0%, P < 0.01), velocity (-17.0% +/- 3.7%, P < 0.01), and RBF (-29.4% +/- 4.6%, P < 0.01) significantly decreased compared with the preinjection level. In the PBS group, maximum increases above the prehypoxia diameter (13.7% +/- 3.5%, P < 0.01), velocity (39.5% +/- 8.6%, P < 0.01), RBF (73.9% +/- 10.6%, P < 0.01), and WSR (28.3% +/- 7.1%, P < 0.01) were observed during hypoxia. In the L-NAME group, those changes substantially decreased in response to hypoxia. D-NAME was inactive with regard to RBF during rest and hypoxia.

These results suggest that NO may be continuously produced in the retina during rest and contributes to increased RBF during hypoxia. In addition, the increased WSR during hypoxia indicates that NO plays an important role in retinal hypoxic hyperemia through a flow-induced mechanism.