Clinical Hemorheology and Microcirculation - Volume 12, issue 1
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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: Intravital videomicroscopy was used to investigate interactions between blood platelets, vascular cells and leukocytes at a site of vessel wall injury in rabbit mesenteric venules (diameter 21–40 μm). A thromboembolic reaction was evoked by puncture of the wall with a glass micropipet (tip 6–8 μm); in all vessels a thrombus was formed, while in most vessels emboli were produced as well. Leukocyte rolling, i.e. their movement along the wall at a clearly lower velocity than the other blood cells flow, was quantitated simultaneously in vessel segments upstream and downstream of a thrombus. In venules without embolization the degree of leukoycte…rolling was not different upstream and downstream of the thrombus, indicating that fluid dynamic changes induced by the thrombus do not influence leukocyte rolling. In venules, in which emboli were produced, leukocyte rolling decreased significantly from upstream to downstream of the thrombus during embolization (median decrease: 45%; p≤0.001). This decrease in leukocyte rolling still existed after embolization had stopped (50%; p≤0.01), indicating that it cannot be explained by inclusion of leukocytes in emboli. Inhibition of prostaglandin formation with aspirin (100 mg/kg) significantly diminished the influence of the thromboembolic reaction on leukocyte rolling (p≤0.05), but blockade of TXA2 -receptors with sulotroban (30 mg/kg) had no effect. The findings suggest that substances, produced by activated blood platelets and/or damaged vascular cells, diminish leukocyte rolling. The identity of the substances is not yet clear, but prostaglandins, other than TXA2 , are probably involved.
Abstract: Cytokine produce important effects on polymorphonuclear (PMN) functions. We have studied PMN functions in patients with acute inflammatory syndrome with endogenous production of cytokines due to myocardial infarction (MI) at D1 and D3 and in patients suffering from neoplasia submitted to different in vivo cytokines administration: Interleukine 2 (IL-2), Interferon gamma (IFN-G), association IL-2/IFN-G, Granulocyte-colony stimulating factor (G-CSF) before (D0) and at the end of treatment (D36). In MI, leukocyte count increased on the first day and decreased at 03 certainly due to plugging and local destruction. Leukocyte activation occured at 01 and was more pronounced at D3. The…in vivo administration of cytokines had contradictory effects: – IL-2 had a significant inhibitory effect on directed chemotaxis at the end of treatment (D36), while the other functions were not modified. – INF-G had no effect. – This inhibitory effect of IL-2 was not observed when IFN-G was administrated together with IL-2. – G-CSF induced the most important activation of PMN.
Abstract: Ischemia-reperfusion is associated with activation of leukocytes which accumulate in the postischemic tissue, adhere to the microvascular endothelium, emigrate into the perivascular space and contribute to postischemic reperfusion injury through the release of cytotoxic enzymes as well as generation of oxygen free radicals. In the following we have summarized the results of four studies in which the effects of different pharmacological agents on leukocyte-endothelium interaction after ischemia-reperfusion were tested. A 4h ischemia was induced to a thin striated muscle contained in the dorsal skin fold chamber preparation of awake hamsters. Using intravital fluorescence microscopy and a computer-assisted microcirculation analysis system,…red cell velocity, vessel diameter, and leukocyte-endothelium interaction were analyzed in postcapillary venules. Drugs under investigation were infused intravenously prior to and during the early phase of reperfusion. Animals received either adenosine (110 μg kg−1 min−1 ), buflomedil (3 mg kg−1 body weight), the selective leukotriene synthesis inhibitor MK-886 (20 μmol kg−1 h−1 ), or dextran 70 (5 mg kg−1 body weight). In saline-treated control animals, a drastic increase of leukocyte sticking and rolling along the endothelium was observed in the early phase of reperfusion. In animals treated with adenosine, buflomedil, MK-886 or dextran 70 postischemic leukocyte-endothelium interaction was markedly reduced. Our results indicate a protective pharmacological potential of adenosine, buflomedil, MK-886 and dextran 70 on postischemic leukocyte adhesion to the endothelium of postcapillary venules.
Keywords: Microcirculation, ischemia-reperfusion, leukocyte, endothelium, drug action
Abstract: Perfluorochemicals are substances with a small particle size, low viscosity, and high oxygen-carrying capacity. We have investigated the role of one perfluorochemical, Fluosol, an emulsion of two perfluorocarbons, a detergent [Pluronic F-68], and phospholipids on myocardial reperfusion injury in the closed-chest canine model. Intracoronary and intravenous Fluosol infused in the peri-reperfusion period significantly reduced infarct size and improved ventricular function up to two weeks after reperfusion. Fluosol attenuates neutrophil infiltration into the reperfused bed, preserves endothelial cell structure, and reduces neutrophil plugging of capillaries. Endothelium-dependent relaxation of large and small vessels was maintained 1 hour after reperfusion in Fluosol animals.…Ex vivo studies showed apparent suppression of neutrophil chemotaxis and lysozyme degranulation. Unstimulated neutrophils manifested enhanced superoxide anion production within 5 minutes of incubation even with low concentrations of Fluosol, and this effect was almost entirely due to Pluronic F-68. Neutrophil stimulation was prevented by cytochalasin B, an inhibitor of phagocytosis. Perfluorochemicals may offer a novel therapy to enhance myocardial salvage after successful reperfusion. The mechanism appears to be due to “deactivation” of neutrophils peripherally, thereby reducing their cytotoxic potential in the reperfused myocardium.
Abstract: Perfluorochemicals (PFCs) are valuable in medicine, primarily as 02-carrying perfusates and tissue imaging agents. Their basic properties are described, including the need for emulsification before intravascular use. The formulation and assessment of PFC emulsions and their components in man and other species are discussed. Attention is focussed on the use of the commercial emulsion, Fluosol™ during clinical coronary angioplasty. Potential applications for PFCs in cancer therapy, ophthalmology, and the treatment of blood and respiratory disorders are also outlined.