Biomechanical and morphological differences between the sclera canal ring and a peripheral sclera ring in the porcine eye.

AIM: To investigate a possible association between the biomechanical load and unload behaviour and the elastin content of the sclera canal ring (SCR) and a superiorly localized sclera ring (SPS) in the porcine eye. METHODS: Two sclera rings were trephined from each of 40 porcine eyes, one containing the SCR and the other an SPS. The load and the unload curves were measured in the extension range of 0-2.0 mm by a biomaterial tester. Hysteresis was determined from the area enclosed by the loading and unloading curve. Histochemical staining with resorcin-fuchsin and morphometric analysis of paraffin-embedded sections of both rings were performed to detect the area occupied by elastin fibres. RESULTS: At 1 mm extension, the mean load of the SCR was 0.89 ± 0.22 N and that of the SPS 1.13 ± 0.19 N, which was not significantly different between both rings (p > 0.05). Mean hysteresis in the SCR was 1.55 ± 0.30 N × mm and 1.90 ± 0.18 N × mm in the SPS, which was significantly different between both rings (p = 0.01). Mean sclera thickness was 986 µm in the SCR (range: 900-1,060 µm) and 971 µm in the SPS (range: 800-1,200 µm) without a statistically significant difference between both sclera rings (p = 0.78). The area occupied by elastin fibres was 15.5 ± 3.4% in the SCR and 4.5 ± 1.5% in the SPS, which was significantly different between both rings (p = 0.0001). CONCLUSION: Hysteresis in the SCR was significantly lower than in the SPS, indicating a higher elasticity of the SCR in the porcine eye. This effect could be explained by a higher content of elastin in the surrounding ring of the peripapillary optic nerve head providing reversible contraction in cases of intra-ocular pressure variations.

Diabetes mellitus affects biomechanical properties of the optic nerve head in the rat.

BACKGROUND: To investigate the effect of diabetes on the biomechanical behavior of the optic nerve head (ONH) and the peripapillary sclera (ppSc) in streptozocine-induced diabetic rats. METHODS: Diabetes mellitus was induced in 20 Wistar rats using streptozocine. Twenty-five nondiabetic rats served as controls. Eyes were enucleated after 12 weeks and 2 strips of one eye were prepared containing ONH or ppSc. The stress-strain relation was measured in the stress range of 0.05-10 MPa using a biomaterial tester. RESULTS: At 5% strain the stress of the ONH in diabetic rats was 897±295 kPa and in the control group it was 671±246 kPa; there was a significant difference between both groups (p=0.011). The stress of the diabetic ppSc (574±185 kPa) increased compared to that of the nondiabetic ppSc (477±171 kPa), but this did not reach statistical significance (p=0.174). The calculated tangent modulus at 5% strain was 11.79 MPa in the diabetic ONH and 8.77 MPa in the nondiabetic ONH; there was a significant difference between both groups (p=0.006). The calculated tangent modulus at 5% strain was 7.17 MPa in the diabetic ppSc and 6.12 MPa in the nondiabetic ppSc, without a statistically significant difference (p=0.09). CONCLUSION: In contrast to the ppSc, the ONH of diabetic rats showed a significant increase in stiffness compared to nondiabetic rats, which might be explained by nonenzymatic collagen cross-linking mediated by advanced glycation end products due to high blood glucose levels in diabetes. Further studies are needed to investigate if these biomechanical changes represent a detrimental risk factor for intraocular pressure regulation in diabetic glaucoma patients.

Statins affect ocular microcirculation in patients with hypercholesterolaemia.

PURPOSE: To investigate the effect of statins on ocular microcirculation in patients with hypercholesterolaemia. METHODS: Ten patients with hypercholesterolaemia were included in this study. The diameter of retinal vessels was measured continuously with the retinal vessel analyser (RVA) before and 4 weeks after statin therapy. After baseline assessment, a monochromatic luminance flicker was applied to evoke retinal vasodilation. Flicker response was then analysed after 50, 150 and 250 seconds after baseline measurement. Additionally, cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglyceride levels were obtained to find a possible correlation between retinal vessel diameter changes and lipid metabolism before and after statin therapy. RESULTS: The mean diameter of the arterioles before statin therapy at baseline was 106.3 ± 1.5 µm and the mean diameter of the venules at baseline was 127.3 ± 2.5 µm. The mean diameter of the arterioles 4 weeks before statin therapy was 107.3 ± 1.8 µm after 50 seconds, 107.9 ± 1.8 µm after 150 seconds and 108.0 ± 1.8 µm after 250 seconds (p = 0.01). The mean diameter of the venules 4 weeks before statin therapy was 128.0 ± 2.6 µm after 50 seconds, 128.2 ± 2.5 µm after 150 seconds and 128.2 ± 2.3 µm after 250 seconds (p = 0.01). The mean diameter of the arterioles 4 weeks after statin therapy at baseline was 107.1 ± 1.6 µm and the mean diameter of the venules at baseline was 127.7 ± 2.3 µm which was significantly different from measurements before statin therapy (p = 0.004). The diameter of the arterioles 4 weeks after statin therapy increased to 109.2 ± 2.1 µm after 50 seconds, to 110.6 ± 2.6 µm after 150 seconds and to 111.8 ± 2.3 µm after 250 seconds with statistical significance at all time points (p = 0.001). The mean diameter of the venules after statin therapy increased to 130.6 ± 2.7 µm after 50 seconds, to 132.1 ± 2.6 µm after 150 seconds and to 133.5 ± 3.0 µm after 250 seconds with statistical significance at all time points (p = 0.001). CONCLUSIONS: The present study demonstrated a significant increase in vasodilatation of retinal arterioles and venules 4 weeks after statin therapy in patients with hypercholesterolaemia indicating pleiotropic effects of statins on the retinal microcirculation which seem to be mediated by the endothelium-dependent, NO-mediated pathway.