Clinical Hemorheology and Microcirculation - Volume 13, issue 5
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Clinical Hemorheology and Microcirculation, a peer-reviewed international scientific journal, serves as an aid to understanding the flow properties of blood and the relationship to normal and abnormal physiology. The rapidly expanding science of hemorheology concerns blood, its components and the blood vessels with which blood interacts. It includes perihemorheology, i.e., the rheology of fluid and structures in the perivascular and interstitial spaces as well as the lymphatic system. The clinical aspects include pathogenesis, symptomatology and diagnostic methods, and the fields of prophylaxis and therapy in all branches of medicine and surgery, pharmacology and drug research.
The endeavour of the Editors-in-Chief and publishers of
Clinical Hemorheology and Microcirculation is to bring together contributions from those working in various fields related to blood flow all over the world. The editors of
Clinical Hemorheology and Microcirculation are from those countries in Europe, Asia, Australia and America where appreciable work in clinical hemorheology and microcirculation is being carried out. Each editor takes responsibility to decide on the acceptance of a manuscript. He is required to have the manuscript appraised by two referees and may be one of them himself. The executive editorial office, to which the manuscripts have been submitted, is responsible for rapid handling of the reviewing process.
Clinical Hemorheology and Microcirculation accepts original papers, brief communications, mini-reports and letters to the Editors-in-Chief. Review articles, providing general views and new insights into related subjects, are regularly invited by the Editors-in-Chief. Proceedings of international and national conferences on clinical hemorheology (in original form or as abstracts) complete the range of editorial features.
The following professionals and institutions will benefit most from subscribing to
Clinical Hemorheology and Microcirculation: medical practitioners in all fields including hematology, cardiology, geriatrics, angiology, surgery, obstetrics and gynecology, ophthalmology, otology, and neurology. Pharmacologists, clinical laboratories, blood transfusion centres, manufacturing firms producing diagnostic instruments, and the pharmaceutical industry will also benefit.
Important new topics will increasingly claim more pages of
Clinical Hemorheology and Microcirculation: the role of hemorheological and microcirculatory disturbances for epidemiology and prognosis, in particular regarding cardiovascular disorders, as well as its significance in the field of geriatrics. Authors and readers are invited to contact the editors for specific information or to make suggestions.
Abstract: Recent evidence suggests that shear-induced platelet aggregation (SIPA) is an important mechanism of thrombosis at arterial bifurcations or stenotic lesions. We measured SIPA using newly-developed equipment in patients with cerebral ischemia, and also studied the effects of various pharmacological agents on SIPA in vitro and ex vivo. Platelet aggregation was induced by high shear stress (108 dyne/cm2 ), which is dependent on von Willebrand factor and on glycoproteins IIb/ IIIa and Ib. In vitro studies, SIPA was inhibited by agents that increase the activity of adenylate cyclase as well as inhibitors of platelet ionized calcium, ADP receptor and Gj protein.…but it was not affected by inhibitors of cyclooxygenase, lipoxygenase, thromboxane A2 synthetase, or platelet-activating factor. An increase of SIPA was observed in patients with atherothrombotic stroke and transient ischemic attacks, but not in those with lacunar stroke. SIPA was more often increased in patients who showed an increase of larger von Willebrand factor multimers on SDS agarose gel electrophoresis. Oral aspirin did not inhibit SIPA, but oral ticlopidine significantly inhibited it. The above results indicate that SIPA is mediated or regulated by cyclic AMP, cytoplasmic calcium, and ADP, and also indicate that SIPA is increased in some subtypes of cerebral ischemia, and can be corrected by ticlopidine but not by aspirin.
Abstract: A technique based on Fraunhofer diffraction by suspended particles is applied in this paper to develop a numerical process to assess information about the erythrocyte deformability distribution over a population of more than six millions cells. The ability to evaluate the full distribution rather than just a mean deformability of erythrocytes allows better assessment of the erythrocyte rheologic capabilities. In order to determine both standard deviation and mean of erythrocyte population deformability, the experimental profile of intensities was matched with a theoretical one. This theoretical profile has been drawn by combining theoretical intensities corresponding to the dimensions of each deformed…cell class and assuming a normal distribution. The method has been verified by analyzing mixtures of known proportions of normal erythrocyte and hardened spherocytes. Normal and pathological erythrocytes population were also analyzed and their respective deformability distributions are presented.
Abstract: We tested the accuracy and the usefulness of the MT90 (falling ball) viscometer as an alternative to more expensive and sophisticated devices for physiological and clinical investigations. This instruments measures viscosity from the velocity of a ball falling through a syringe filled with less than 1 ml of blood or plasma at a shear rate of 1000 s-1, i.e. the range of the so-called ‘newtonian’ behavior of blood. We postulated that this shear rate allows us to measure RBC rigidity in a completely disaggregated structure. Four indices of RBC rigidity derived from high shear rate viscometry were used: μ45r (i.e.…blood viscosity at corrected hematocrit 45% divided by plasma viscosity); ‘Tk’ (Dintenfass); ‘k’ (Quemada); ‘μ(RBC)’ (Breugel and coll.). All were strongly correlated to each other (r=0.98 p<0.01) and easily detected in vitro rigidification of RBCs with (a) ionophore A23187 (10−4 M); (b) heating at 56°C during 10 min; (c) 30 min incubation in hypercalcemic-hyperosmolar buffer, when used together with Hanss' hemorheometre. At this shear rate, modifications of blood viscosity induced by changes (within a physiological range) of hematocrit and RBC rigidity were correctly described by both Quemada's and Dintenfass's equations for blood viscosity. ‘k’ values given by the equation of Quemada at this shear rate correlated with RBC rigidity indices calculated with the Carri-Med rheometer using both Quemada's and Wang's equations. Correlations between these indices of rigidity and those given by the hemorheometre were found only for in vitro experiments of RBC stiffening, while in clinical situations viscometric and hemorheometric indices gave rather different results. The coefficient of variation for viscometric measurements was 2% (plasma viscosity) and 3% (blood viscosity). We conclude that this viscometer gives results consistent with other methods. We suggest that it is useful and accurate for physiological and clinical studies.
Abstract: The performance of nickel and polycarbonate micropore filters (both with 5μm pore diameters) were compared using two different blood filtration methods in control and diabetic subjects. Significant differences were detected between these subject groups with nickel filters but not with polycarbonate filters. The coefficients of variation with both filtration methods were lower with the nickel filters, possibly due to their better pore geometry. It is concluded that Veco nickel filters are superior to Nucleopore polycarbonate filters when assessing blood filtration in clinical studies.