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Purpose: To test the hypothesis that blood flow autoregulation in the optic nerve head has less reserve to maintain normal blood flow in the face of blood pressure-induced ocular perfusion pressure decrease than a similar magnitude intraocular pressure-induced ocular perfusion pressure decrease., Materials and Methods: Twelve normal non-human primates were anesthetized by continuous intravenous infusion of pentobarbital. Optic nerve blood flow was monitored by laser speckle flowgraphy. In the first group of animals (n = 6), the experimental eye intraocular pressure was maintained at 10 mmHg using a saline reservoir connected to the anterior chamber. The blood pressure was gradually reduced by a slow injection of pentobarbital. In the second group (n = 6), the intraocular pressure was slowly increased from 10 mmHg to 50 mmHg by raising the reservoir. In both experimental groups, optic nerve head blood flow was measured continuously. The blood pressure and intraocular pressure were simultaneously recorded in all experiments., Results: The optic nerve head blood flow showed significant difference between the two groups (p = 0.021, repeat measures analysis of variance). It declined significantly more in the blood pressure group compared to the intraocular pressure group when the ocular perfusion pressure was reduced to 35 mmHg (p < 0.045) and below. There was also a significant interaction between blood flow changes and the ocular perfusion pressure treatment (p = 0.004, adjusted Greenhouse & Geisser univariate test), indicating the gradually enlarged blood flow difference between the two groups was due to the ocular perfusion pressure decrease., Conclusions: The results show that optic nerve head blood flow is more susceptible to an ocular perfusion pressure decrease induced by lowering the blood pressure compared with that induced by increasing the intraocular pressure. This blood flow autoregulation capacity vulnerability to low blood pressure may provide experimental evidence related to the hemodynamic pathophysiology in glaucoma.

PURPOSE. To evaluate the effect of acutely elevated intraocular pressure (IOP) on retinal thickness and optic nerve head (ONH) structure in the rat eye by spectral domain-optical coherence tomography (SD-OCT). METHODS. Fourteen adult male Brown-Norway rats were studied under anesthesia (ketamine/xylazine/acepromazine, 55:5:1 mg/kg intramuscularly). Both eyes were imaged by SD-OCT on two baseline occasions several weeks before and again 2 and 4 weeks after the acute IOP imaging session. During the acute IOP session, SD-OCT imaging was performed 10 minutes after IOP was manometrically set at 15 mm Hg and then at 10, 30, and 60 minutes after IOP had been elevated to 50 mm Hg (n = 8) and again 10 and 30 minutes after IOP had been lowered back to 15 mm Hg (recovery). In two additional groups, IOP elevation was set to 70 mm Hg (n = 4) or 40 mm Hg (n = 2). Acute IOP results are reported for a pattern of 49 horizontal B-scans spanning a 20° square and follow-up results for peripapillary circular B-scans. Retinal and retinal nerve fiber layer (RNFL) thicknesses were measured with custom software by manual image segmentation. Friedman and Dunn's tests were used to assess acute and longer-term effects of acute IOP elevation. RESULTS. Acute IOP elevation to 50 mm Hg caused rapid (within seconds) deformation of the ONH and peripapillary structures, including posterior displacement of the ONH surface and outward bowing of peripapillary tissue; retinal thickness decreased progressively from 10 to 30 to 60 minutes by 16%, 18%, and 20% within the area of Bruch's membrane opening (BMO; P < 0.0001) by 8%, 9%, and 11% within the central 10° (excluding the BMO; P < 0.0001) but only by 1%, 2%, and 2.4% beyond the central 10° (P < 0.0001). Recovery was progressive and nearly complete by 30 minutes. Acute IOP elevation to 40 and 70 mm Hg produced similar structural changes, but 70 mm Hg also interfered with retinal blood flow. There were no changes in peripapillary retinal or RNFL thickness (P = 0.08 and P = 0.16, respectively) measured 2 and 4 weeks after acute elevation to 50 mm Hg. CONCLUSIONS. Acute IOP elevation in the rodent eye causes rapid, reversible posterior deformation of the ONH and thinning of the peripapillary retina, with only minimal retinal thinning beyond 5° of the ONH. No permanent changes in peripapillary retinal or RNFL thickness (for up to 1 month of follow-up) were caused by 60 minutes of IOP elevation to 50 mm Hg.

Purpose: To determine whether acutely elevated intraocular pressure (IOP) alters peripapillary retinal thickness, retinal nerve fiber layer thickness (RNFLT), or retardance., Methods: Nine adult nonhuman primates were studied while under isoflurane anesthesia. Retinal and RNFLTs were measured by spectral domain optical coherence tomography 30 minutes after IOP was set to 10 mm Hg and 60 minutes after IOP was set to 45 mm Hg. RNFL retardance was measured by scanning laser polarimetry in 10-minute intervals for 30 minutes while IOP was 10 mm Hg, then for 60 minutes while IOP was 45 mm Hg, then for another 30 minutes after IOP was returned to 10 mm Hg., Results: RNFLT measured 1120 microm from the ONH center decreased from 118.1 +/- 9.3 microm at an IOP of 10 mm Hg to 116.5 +/- 8.4 microm at 45 mm Hg, or by 1.4% +/- 1.8% (P < 0.0001). There was a significant interaction between IOP and eccentricity (P = 0.0006). Within 800 microm of the ONH center, the RNFL was 4.9% +/- 3.4% thinner 60 minutes after IOP elevation to 45 mm Hg (P < 0.001), but unchanged for larger eccentricities. The same pattern was observed for retinal thickness, with 1.1% +/- 0.8% thinning overall at 45 mm Hg (P < 0.0001), and a significant effect of eccentricity (P < 0.0001) whereby the retina was 4.8% +/- 1.2% thinner (P < 0.001) within 800 microm, but unchanged beyond that. Retardance increased by a maximum of 2.2% +/- 1.1% 60 minutes after IOP was increased to 45 mm Hg (P = 0.0031)., Conclusions: The effects of acute IOP elevation on retinal thickness, RNFL thickness and retardance were minor, limited to the immediate ONH surround and unlikely to have meaningful clinical impact.