The retinal hemodynamic responses to intravitreal injection of
10
−3 M
l-NMMA
or 10
−4 M BQ-788 alone in
nondiabetic rats are presented in
Table 2 . After NOS inhibition, there were no significant retinal hemodynamic
changes at 15 minutes or 30 minutes; however, 40 minutes after
injection, there was a significant decrease in retinal blood flow
compared with baseline measurements (77.5 ± 18.2
pixel
2/sec;
P < 0.05; data not
shown). After injection of the ETB antagonist, retinal blood flow was
significantly decreased 15 minutes after injection (
P < 0.05) and at 30 minutes reverted to flows comparable to baseline.
The retinal response to
10
−8 M ET-3 in nondiabetic
rats after a 15-minute pretreatment with
10
−3 M
l-NMMA
(
n = 6), 10
−4 M
BQ-788 (
n = 6), or vehicle (
n = 6) is summarized
in
Figure 3 . In the eyes pretreated with vehicle alone, the expected biphasic
retinal blood flow response to ET-3 was measured with a rapid transient
increase in retinal blood flow (173.6 ± 71.0
pixel
2/sec compared with baseline 101.6 ±
29.4 pixel
2/sec;
P < 0.05) 2
minutes after ET-3 injection, followed by a reduction in retinal blood
flow 15 minutes after ET-3 injection (86.1 ± 49.8
pixel
2/sec). In the eyes pretreated with the NOS
inhibitor
l-NMMA, the characteristic blood flow
response to ET-3 was completely inhibited. Blood flow at 2 minutes
(98.3 ± 31.7 pixel
2/sec) was significantly
decreased compared with that in vehicle-pretreated eyes (173.6 ±
71.0 pixel
2/sec;
P < 0.05).
Similarly, in the eyes pretreated the ETB antagonist (BQ-788) the
characteristic retinal blood flow response to ET-3 was significantly
inhibited (
P < 0.02, compared with vehicle pretreated
eyes). BQ-788 pretreatment also significantly reduced retinal blood
flow (74.9 ± 20.3 pixel
2/sec) compared with
baseline (108.9 ± 38.4 pixel
2/sec;
P < 0.05) before intravitreal ET-3 injection.