Clinical Hemorheology and Microcirculation

To study the microrheological characteristics of RBCs during erythrocyte senescence in vivo, an anemia model of rabbit induced by phenylhydrazine injection was developed. Measurements of the hematocrit, the deformation indexes, the blood viscosity and the sedimentation, etc. were performed in vivo for more than 60 days in the processes of RBC senescence. Obvious changes in the RBC's rheological characteristics were found in this senescent model. Compared with our previously developed Wen's model [1,2] in which the entire RBC population was nearly synchronously produced following the induction of spherocytic anemia in the rabbit with antibody serum, the changes of RBC microrheological characteristics for this model showed approximately the same tendency, although Wen's model with antibody serum was much better in its ability to simulation of the nearly normal physiological conditions than the present one with phenylhydrazine injection. Hence, the present model can serve as a model of RBC senescence under abnormal physiological conditions.

It is already admitted that hormone replacement therapy (HRT) decreases the risk of developing cardiovascular disease, although its mechanism is not clear yet. In the present work, the effect of the HRT upon cellular and plasmatic haemorheological factors determining blood flow properties: blood viscosity, plasma viscosity, plasma fibrinogen, rigidity erythrocyte index and erythrocyte aggregation rate was studied. Menopausal women were followed through a whole year of HTR.

Results demonstrate that after six months of treatment there is a diminution in relative blood viscosity and erythrocyte rigidity, with constant values along the second semester. Erythrocyte aggregation, plasmatic and blood viscosity diminution observed during the treatment can be explained by the simultaneous plasma fibrinogen decrease.

Modified cellular and plasmatic rheology could produce beneficial effects on blood flow, particularly in microcirculation, presenting a possible mechanism by which HTR decreases the risk of cardiovascular disease development during menopause.

The aim of this work was to study the red cell morphology in different stages of schistosomiasis. Patients were divided into three groups according to the stage of the disease. For each patient, complete clinical examination, liver function tests, renal function tests, complete blood picture, scanning electron microscopy for erythrocytes (SEM) and abdominal ultrasonography were done. Abnormal morphologic changes of a total discoid flat cells of 70.14%, margin changes of 12.34% and 3.55% of cup forms were found. To our knowledge, these marked changes were not reported in any other disease. No statistical differences were found between red cell shape changes and stage of liver disease. There was a positive correlation between portal vein diameter and percentage of flat discoid forms and a negative correlation between surface changes and clinical stage of liver disease. These changes are known to be accompanied by reduction of red cell deformability and impaired capillary flow.

The present investigation was designed to evaluate the acute effect of aerobic exercise on oxidative stress and the flow properties of the blood. Fourteen clinically healthy subjects (7 men and 7 women aged 56±19 yr) underwent maximal treadmill exercise with blood samples drawn prior to and immediately after exercise. Post‐exercise significant increases were observed in plasma lipid hydroperoxides from 6.5±2.0 μM to 7.9±1.9 μM (p<0.0001) and the relative concentration of plasma fluorescent products associated with red cell peroxidation from 138±28 RF to 220±92 RF (p<0.005). After exercise there was a rise in the hematocrit from 41.4±3.7% to 44.4±4.1% (p<0.0001), increases in whole blood viscosity at shear rates of 22.5/sec to 450/sec (p<0.0005), an increase in plasma viscosity from 1.27±0.12 cP to 1.36±0.11 cP (p<0.01), an increase in red cell rigidity from 2.44±0.48 cP to 2.62±0.42 cP (p<0.001) and a decrease in erythrocyte sedimentation rate from 26.9±18.6 mm/h to 22.5±15.9 mm/h (p<0.01). The findings suggest that acute aerobic exercise induces oxidative damage to red blood cells and adversely affects rheological properties of the peripheral blood.

This study investigated the impact of oral fluid intake on blood rheology of 17 healthy adults following a 12–14 hour overnight fast from food and drink. An oral fluid load of 500 ml was consumed every 30 minutes for 2 hours. Blood viscosity values at shear rates of 1, 10 and 100 s⁻¹ were reduced (p<0.05 to p<0.01) at 30 and 120 minutes following hydration; however, these differences were not significant after hematocrit correction. With fluid intake, both uncorrected and corrected viscous component of blood viscoelasticity at oscillatory shear rate of 1 s⁻¹ and at a constant frequency of 2 Hz were reduced (p<0.05 to p<0.001) at all time points as compared to fasting values. The corrected elastic component of blood viscoelasticity increased 90 minutes after hydration (p<0.05). An overnight fast is accompanied by rheological abnormalities that are altered by fluid intake.

A complete neurological and laboratory assessment was made of 31 transient ischemic attack (TIA) and 33 acute ischemic stroke patients. Laboratory parameters were compared with 33 age‐ and sex‐matched controls. Erythrocyte deformability was characterised by determining the relative cell transit time (RCTT) with a St. George filtrometer. Plasma viscosity was measured with a Haake microviscosimeter. In comparison with controls, fibrinogen content, erythrocyte sedimentation rate (ESR), platelet and leukocyte count, erythrocyte RCTT and plasma viscosity were found to be significantly higher in stroke patients. In TIA patients the elevation of these values was not significant with the exception of platelet count. Our results suggest that the hemorheological alterations observed in TIA and stroke are largely non‐specific findings and associated with the atherosclerotic disease of patients. The significant elevation of leukocytes, fibrinogen and plasma viscosity in acute stroke versus TIA probably reflects the systemic acute phase response of organism to cerebral infarction.

Cerebral microvascular changes due to air embolism‐reperfusion in the cat were investigated. Air embolism‐reperfusion was produced in the cerebral microvessels by an intra‐carotid injection of air (0.2–0.3 ml). Air emboli in the cerebral arterioles were observed continuously from the air injection to reperfusion using fluorescence videomicroscopy. Arteriolar diameter was measured based on video images of arterioles filled with rhodamine‐B isothiocyanate dextran, and red cell velocity was measured using a dual window technique with FITC‐labeled red cells. Air bubbles ceased to move in the arterioles of 20–70 μm diameter and blood flow was almost stopped in distal arterioles. The air emboli were of cylindrical shape in the arterioles, with hemispherical end caps. The emboli progressed slowly at rates of 7–73 μm/sec and then flowed away. The air emboli induced ischemia‐reperfusion with the ischemic duration of approximately 1 minute (10 sec–3 min) at the arteriolar level. Cerebral arterioles began to dilate after the formation of the air emboli and significantly dilated by approximately 50% after reperfusion. A transient increase in red cell velocity was observed after reperfusion. Arteriolar dilation and the increase in velocity led to a hyperemic response in arteriolar flow to ischemia‐reperfusion.