BACKGROUND:This study aimed to evaluate the ratio of C-reactive protein (CRP) to albumin, inflammatory markers, and parameters from the complete blood count (CBC) in patients with Takayasu arteritis and the association with disease activity. MATERIAL...
Background:This experiment was performed to compare the effects of Phenytoin (PHT) and Hypericin (HP) cream on healing of burn wounds in rats. Material andMethods:Twenty rats were divided into 3 groups and second-degree burn wounds were created. The ...
1 January 2011 in Clinical Hemorheology and Microcirculation
Acrylamide which is formed via reaction of reducing sugars with amino acids during food processing at high temperatures is not only neurotoxic and carcinogenic, but it also damages erythrocyte membrane and generates micronucleated erythrocytes. In the present study, effects of chronic administration of acrylamide at a dose which does not induce neurotoxicity were evaluated on blood viscosity parameters (hematocrit, erythrocyte deformability, erythrocyte aggregation and plasma viscosity). Twenty adult male Sprague-Dawley rats were divided into control and acrylamide groups. The acrylamide group received 10 mg/kg/day acrylamide, whereas the control group received saline (vehicle), both in 10 ml/kg/day volume via gastric gavage. Erythrocyte aggregation and deformability were measured with LORCA and plasma viscosity with cone-plate viscometer. Erythrocyte deformability was measured before, and at the end of the 3rd and the 5th weeks of acrylamide administration. Hematocrit, erythrocyte aggregation and plasma viscosity were measured only at the end of the 5th week. Acrylamide caused a significant decrease in the deformability index of erythrocytes (at the end of the 3rd week, control: 0.606 ± 0.003, acrylamide: 0.595 ± 0.003, p < 0.05) (at the end of the 5th week, control: 0.606 ± 0.002, acrylamide: 0.588 ± 0.002, p < 0.01). Aggregation tendency and plasma viscosity were slightly higher in the acrylamide group, however the difference was not statistically significant. These results imply that acrylamide which does not cause neurotoxicity in rats may alter blood viscosity if chronically taken.
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.