Abstract
Purpose: :
To investigate the regulatory mechanism of retinal circulation during decreased ocular perfusion pressure (OPP) in cats.
Methods: :
The effect of acute decreased OPP on retinal arteriolar diameter (D), flow velocity (V) and blood flow (RBF) was assessed with laser Doppler velocimetry. We manipulated the OPP by either elevated intraocular pressure (IOP) or systemic hypotension. The involvements of nitric oxide (NO), adenosine and/or N-methyl-D-aspartic acid (NMDA) in the regulation of retinal arteriolar hemodynamics during decreased OPP were determined at two hours after intravitreal injections of respective inhibitors.
Results: :
The OPP was gradually decreased from 90 to 40 mmHg. In the PBS group, the V decreased in proportion to the decreased OPP whereas the D gradually increased. As a result, RBF was maintained at more than 70 mmHg of OPP but significantly decreased less than 60 mmHg of OPP during decreased OPP by both elevated IOP and systemic hypotension. 8-(p-Sulfophenyl)theophylline hydrate (8SPT; an adenosine receptor blocker) also enhanced the reduced RBF in response to both elevated IOP and systemic hypotension whereas Nω-nitro-L-arginine methylester (L-NAME; NO synthase inhibitor) and DL-2-Amino-5-phosphonopentanoic acid (DL-APV; an NMDA receptor antagonist) enhanced the decreased RBF in response to only elevated IOP.
Conclusions: :
Our data suggest that the RBF may be maintained at more than 70 mmHg of OPP. In addition, NO, adenosine and NMDA may be responsible for the RBF preservation in response to the decreased OPP by elevated IOP whereas adenosine may be responsible in response to that by systemic hypotension, suggesting that different vasoregulatory factors may regulate the retinal microcirculation during the decreased OPP between elevated IOP and systemic hypotension.
Keywords: blood supply • retina • oxygen