As a preliminary experiment, only nilvadipine solvent (0.2 mL/kg) was administrated and its influence was studied (n = 8). BP gradually decreased after induction of general anesthesia in one monkey, possibly caused by systemic factors. Data for that particular monkey were then excluded from subsequent analysis. BP showed little change during the experiment (P > 0.30) in the remaining seven monkeys, NBONH showed little change in both eyes during the experiment (P = 0.24), while the pulse rate gradually decreased (between 30 and 60 minutes after the injection, P = 0.007–0.031), and the IOP at 60 minutes was approximately 4 to 6 mm Hg lower than before injection in both laser-treated (P = 0.012) and control (P = 0.024) eyes.
In the lomerizine experiment, BP showed gradual decrease in one monkey, for which data were excluded. In eight monkeys, BP showed no apparent change during the experiment, but the HR gradually decreased (at 50–60 minutes after the injection,
P = 0.036–0.039;
Fig. 2A). Before the lomerizine injection, IOP was 24.1 ± 7.1 and 14.8 ± 3.5 mm Hg (mean ± SD,
n = 8) in the treated and control eyes, respectively, with significant intereye difference (
P = 0.006), and at 60 minutes, it significantly decreased to 18.4 ± 4.2 (
P = 0.002) and 11.2 ± 2.1 (
P = 0.002) mm Hg with significant intereye difference (
P = 0.003). Ocular perfusion pressure (OPP) calculated as (2/3 × (mean brachial BP) – IOP) was 6.2 ± 10.4 and 15.5 ± 6.2 mm Hg before injection, and 11.8 ± 6.3 and 19.0 ± 6.1 mm Hg at 60 minutes, respectively, with significant intereye differences (
P = 0.006 and
P = 0.003, respectively).
The measured NB
ONH values were 10.1 ± 2.2 and 9.6 ± 1.5 before injection in the experimental glaucoma and control eyes, respectively. It increased by 7% at 10 minutes (
P = 0.033) in the experimental glaucoma eye, and by 15% at 10 minutes (
P = 0.039) in the controls with significant intereye difference at 30 and 40 minutes (
P = 0.032 and 0.080;
Fig. 2B). The NB
ONH AUC was 221 ± 399 in arbitrary units in the experimental glaucoma, and 582 ± 488 in the control eyes, respectively, with significant intereye difference (
P = 0.036).
In the nilvadipine experiment, BP showed gradual apparent decrease in two monkeys, of which data were excluded. In seven monkeys, HR showed no apparent change during the experiment, but then gradually declined (at 10, 20, 40, and 60 minutes after the injection,
P = 0.0017–0.028;
Fig. 3A). Before nilvadipine injection, IOP was 18.9 ± 2.9 and 14.0 ± 2.5 mm Hg (mean ± SD,
n = 7) in the experimental glaucoma and untreated eyes, respectively, though intereye difference was insignificant (
P = 0.072), and at 60 minutes, it decreased to 11.3 ± 2.7 (
P = 0.008) and 9.7 ± 2.5 (
P = 0.034) mm Hg. OPP was 11.8 ± 2.7 and 16.7 ± 3.9 mm Hg before injection and 22.7 ± 4.5 and 24.3 ± 4.8 mm Hg at 60 minutes in the experimental glaucoma and control eyes, respectively, with no significant intereye difference at both time points.
The measured NB
ONH were 9.8 ± 2.6 and 9.0 ± 1.0 before the injection in the glaucomatous and untreated eyes, respectively. It slightly increased by 3% at 10 minutes (
P = 0.044 without Bonferroni's correction) in the experimental glaucoma eye, while it increased by 12% at 5 to 10 minutes in the controls (
P = 0.013 and 0.008) with a significant intereye difference at 10 minutes (
P = 0.008;
Fig. 3B). NB
ONH AUC was 78.8 ± 72.8 in arbitrary units in the glaucoma, and 230 ± 128 in the untreated eyes, respectively, with significant intereye difference (
P = 0.011).
The results of NBONH response were summarized in the Table.