ABSTRACT.Purpose: To evaluate the ocular blood flow velocities and haemorheological parameters in patients with primary open-angle glaucoma (POAG), exfoliative glaucoma (XFG) and exfoliation syndrome (XFS) and to compare their results with those of healthy controls. Methods: Twenty-five patients with POAG (group 1), 25 patients with XFG (group 2), 25 patients with XFS (group 3) and 25 healthy controls (group 4) were included in the study. Ocular blood flow velocities of ophthalmic artery (OA), central retinal artery (CRA) and short posterior ciliary arteries (SPCAs) were measured using colour Doppler imaging (CDI). Haemorheological parameters (erythrocyte elongation and aggregation index, aggregation amplitude, aggregation half-life, plasma viscosity, haematocrit) were measured in venous blood samples of all patients. Results: The peak systolic velocity (PSV) and end-diastolic velocity (EDV) values were lower and resistive indices (RI) were higher for the OA, CRA and SPCA of glaucomatous (groups 1 and 2) patients compared with those of controls (group 4) (PSV: OA, 40.4 ± 11.3 versus 52.6 ± 12.8 cm ⁄ second, p < 0.001; CRA, 12.9 ± 2.9 versus 15.3 ± 4.2 cm ⁄ second, p = 0.02; SPCA, 21.7 ± 6.6 versus 26.6 ± 8.3 cm ⁄ second, p = 0.013) (EDV: OA, 10.3 ± 4.3 versus 14.2 ± 5.1 cm ⁄ second, p < 0.001; CRA, 3.7 ± 1.1 versus 4.5 ± 1.3 cm ⁄ second, p = 0.025; SPCA, 5.2 ± 1.8 versus 7.7 ± 3.2 cm ⁄ second, p = 0.001) (RI: OA, 0.75 ± 0.05 versus 0.66 ± 0.07, p < 0.001; CRA, 0.73 ± 0.08 versus 0.68 ± 0.10, p = 0.223; SPCA, 0.70 ± 0.10 versus 0.63 ± 0.11, p = 0.004). There were no statistically significant differences between the haemorheological parameters of glaucomatous and non-glaucomatous patients. The reduction in ocular blood flow velocities in groups 1, 2 and 3 were not associated with changes in haemorheological parameters. Conclusion: Our results suggest that impairment of the retrobulbar blood flow in POAG and XFG is not associated with alterations in haemorheological parameters.
Selected hematological parameters and erythrocyte deformability indexes for 16 young male military students were compared before and after a period of exposure to heavy pollution. These students lived in Ankara, which has a serious air pollution problem. The mean sulfur dioxide levels measured at a station proximal to the campus where the students lived were 188 micrograms/m3 and 201 micrograms/m3 during first and second measurements, respectively. During the period between the two measurements, the mean sulfur dioxide level was 292 micrograms/m3. Significant erythropoiesis was indicated by increased erythrocyte counts and hemoglobin and hematocrit levels. Methemoglobin percentage was increased to 2.37 +/- 0.49% (mean +/- standard error) from 0.51 +/- 0.23%. Sulfhemoglobinemia was present in six subjects after the period of pollution, but it was not present in any student prior to this period. Significant increases in erythrocyte deformability indexes were observed after the period of pollution, i.e., from 1.13 +/- 0.01 to 1.21 +/0 0.02, implying that erythrocytes were less flexible, which might impair tissue perfusion.
Oxidative stress decreases the deformability of erythrocytes. Anti-oxidant measures may alleviate, pro-oxidative damage may augment this decrease. Melatonin is reported to exert both anti-oxidant and pro-oxidant properties on erythrocytes. The aim of the present study was to evaluate the effects of melatonin on erythrocyte deformability under oxidative stress conditions induced by the combination of hydrogen peroxide (20 mM) and sodium azide (100 µM). Erythrocyte suspensions were incubated for 10 min with melatonin (1-1000 µM) prior to oxidative stress. Erythrocyte deformability was measured by Laser-assisted Optical Rotational Cell Analyzer (LORCA). Lipid peroxidation was determined via malondialdehyde (MDA) measurements by HPLC. Melatonin alone did not change erythrocyte deformability. Oxidative stress alone decreased the deformability of erythrocytes by 25.8 ± 3.1% (P < 0.05). Melatonin pre-treatment augmented the decrease in erythrocyte deformability but prevented lipid peroxidation. Melatonin (1 µM) did not cause any additional effect on erythrocyte deformability. Higher concentrations (10-1000 µM) further decreased deformability (P < 0.05). Erythrocytes exposed to oxidative stress had MDA levels of 116.3 ± 14.3 µmol/g Hb. Melatonin (1 µM) slightly increased MDA levels, but 1000 µM melatonin reduced it by 35% (P < 0.05). These findings indicate that melatonin exerts antioxidant effect on lipids. Deterioration of erythrocyte deformability may be due to a separate pro-oxidative action on proteins.
Microvascular dysfunction is implicated in the pathogenesis of slow coronary flow (SCF), but less attention has been paid to intrinsic properties of blood that can also impair the microcirculatory flow. In this study we aimed to evaluate the blood viscosity focusing on erythrocyte aggregation, erythrocyte deformability and plasma viscosity in SCF. Thirty-three patients with SCF (21 male, 54 ± 12.8 years) and 23 subjects with normal coronary arteries (13 male, 59 ± 10.3 years) were included in the study. Coronary flow was quantified by means of thrombolysis in myocardial infarction (TIMI) frame count and aggregation and deformability of erythrocytes were measured by an ektacytometer. Plasma viscosity was measured by a cone-plate viscometer. Aggregation amplitude (23 ± 3.8 au vs. 15.7 ± 6.1 au, respectively, p < 0.001) and area A index (area above syllectogram) (153.2 ± 30.7 au.s vs. 124.9 ± 49.3 au.s, respectively, p < 0.01) were higher in SCF patients. Aggregation half-time, aggregation index, elongation index and plasma viscosity values were similar between two groups. Correlation analysis revealed a significant relationship between the TIMI frame count for left anterior descending artery and aggregation amplitude in SCF patients (r = 0.679, p < 0.0001). The result of this study reveals changes in erythrocyte aggregation which may contribute to the pathophysiology of SCF. Larger studies are needed to make more robust conclusions on this issue.
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