Clinical Hemorheology and Microcirculation - Volume 34, issue 1-2
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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.
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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 studies demonstrate that the hepatic sinusoidal endothelial cells (SEC) are a sensitive direct target for early toxicity to acetaminophen (paracetamol, APAP) and this toxicity is exacerbated following a single and multiple week-end type alcoholic binge(s). SEC become swollen and begin to lose the ability to endocytose FITC-FSA, a ligand for the scavenger receptor, as early as 30 minutes after the administration of APAP. Gaps through the SEC appear to be formed by the destruction and/or coalescence of fenestrae and are seen as early as 2 hrs after the administration of APAP which is prior to any evidence of injury…to parenchymal cells. The gaps permit red blood cells to penetrate into the Space of Disse. Subsequently, the sinusoid may collapse or disintegrate reducing blood flow. The gaps are larger and more frequent in ethanol binged animals subsequently treated with APAP. Similar gaps are seen in the early stages of hepatic venoocclusive disease. Administration of a NO donor or a MMP-2 and MMP-9 inhibitor minimizes endothelial injury and red blood cell penetration into the Space of Disse. The injury is exacerbated when an inhibitor of eNOS is administered and minimized when iNOS is inhibited suggesting a protective role for constitutive NO derived from SEC. Both NO and MMPs are known to affect the cytoskeleton of SEC which in turn affects the formation and maintenance of the fenestrae.
Keywords: Liver microcirculation, sinusoidal endothelial cells, toxicants, acetaminophen, in vivo microscopy
Abstract: This article reviews authors' recent studies on hepatic microcirculation with special reference to hepatic arterial system. It is concluded that: (1) Hepatic arterial blood pours into the hepatic sinusoid indirectly via the anastomosis between the terminal hepatic arteriole (THAo) and the portal venule (PVn), and directly through the THAo or the capillaries derived from the arterial capillary network around the bile duct in the portal tract; (2) The steep blood pressure gradient between the THAo and the sinusoid is considered to be maintained not only by the relaxation and contraction of the “precapillary sphincter” at the end of the THAo,…but also by the coordinated dilatation and contraction of two types of sinusoidal endothelial fenestrae (SEF) particularly around the portal tract (zone 1); (3) In the regulation of hepatic sinusoidal microcirculation, the hepatic arterial system may supplementarily provides a driving force to the sinusoidal blood flow for keeping it smooth and constant. The main regulators of the sinusoidal blood flow would be present in the portal venous system. The hepatic artery is essential for supplying oxygen to the sinusoidal blood as well as to the bile ducts, portal venules and nerves in the portal tract.
Abstract: This review focused on a few methodologies which the author, with a background of chemical engineering, has developed in the physiological studies of microcirculation. (1) Fluorescent tracers to visualize mass transfer and hemodynamics: By means of a high sensitive SIT camera equipped in an intravital microscope system, dynamic processes of the permeation of a fluorescent dye from the microvessels through the extravascular space to lymphatics was made to be visualized. Dynamic behaviors of the formed elements were also quantitatively analyzed by the selective fluorescent labeling technique. (2) The dye/light method to induce platelet thrombus in vivo: Intravascular platelet aggregation and…subsequent thrombus formation leading to the complete occlusion of the vessels were produced in the microvasculature by the irradiation of filtered light in combination with the intravascular administration of sodium fluorescein. This method enables quantitative evaluation of thrombus formation process in terms of thrombus formation times. Effects of hemodynamic parameters on thrombogenesis in vivo were quantitatively analyzed. (3) Establishment of peritoneal disseminated tumor model: Colon tumor cells (RCN-9) were inoculated into the peritoneal cavity of male Fischer rats, and the intravital microscopic observation of angiogenic vascular growth accompanying tumor growth was made possible. Dynamic behavior of leukocytes in the microcirculation of solid tumor tissue was visualized using a fluorescent labeling technique combined with the use of a real-time confocal laser-scanning microscope.
Abstract: This paper reviews work on microvascular remodeling that has been done over the past years in our lab. It is not our purpose to fully cover the field; rather we explain our progress in a more or less chronological order. We address physiological and pathological remodeling in resistance vessels, the biomechanics of the vascular wall and the factors that determine vascular caliber. Subsequently, the intimate link between maintained vascular tone and inward remodeling is discussed, and we highlight our view that tone and remodeling form hallmarks in a continuous process of vascular adaptation. Finally, the role of transglutaminases in remodeling…is described.
Abstract: Diabetes mellitus type 2 (T2 DM) is a worldwide pandemic disease. T2 DM and hypertension (HT) are closely related and classified as non-communicable diseases. These conditions represent as part of metabolic syndrome. Ageing is an independent risk factor of both diseases. Accumulation of reactive oxygen species (ROS) or imbalance of ROS and antioxidant system, which cause endothelial dysfunction (ED) through depletion of nitric oxide (NO), is likely to be the main risk factor in ageing, T2 DM and HT. The organ that is rich in capillary blood supply like the islets of Langerhans and renal glomeruli, is theoretically prone to…ED after long exposure to accumulation of various oxidants derived from dietary products, such as superoxide radical (O2 − ), hydroxyl radical (OH), malondialdehyde (MDA) and peroxynitrite (ONOO− ), a potent long lived oxidant and cytotoxic. Preventive measures to correct imbalance of oxidant and antioxidation pathways and the sequential effects should be implemented since birth or childhood period by ways of proper diet, exercise, adequate supply of natural antioxidants and lifestyle modifications.
Keywords: Diabetes mellitus type 2 (T2DM), hypertension, ageing, reactive oxygen species (ROS)
Abstract: Despite numerous reports on the regulation of cerebral arterial blood flow, little work has been done on that of the capillary and venous system. We have examined capillo-venous blood flow in the rat intraparenchymal cerebral cortex, employing a high-speed video confocal fluorescence microscope and our own software (KEIOIS-2) to track individual RBCs and to document velocity changes in single capillaries and veins. We found temporal and spatial heterogeneous changes in capillary RBC density (hematocrit), RBC recruitment, oscillation of capillary flow or vasomotion, and capillary density unrelated to arteriolar diametric changes. In veins, blood flow was also quite variable in time…and space, and at a high frame rate venous blood per se was observed as a moving column of amorphous RBC aggregates with irregular edges; we believe this is the first report of such an observation under physiological conditions. The formation of such intravascular RBC aggregates would enforce slowing of blood flow and vice versa: RBC aggregation was in turn entirely flow-dependent. In rapid venous flow, RBCs appeared as a straight gathering of individually separated and dispersed cells. At capillo-venous junctions, an “RBC pouring” process appeared to occur, with RBCs either being sucked up from the capillary, merging, or being held back in the capillary. Changes in venous blood viscosity due to RBC aggregation are likely to be involved in this process. These findings suggest that the capillo-venous junction somehow participates in the regulation of appropriate tissue capillary flow in toto.
Abstract: Many blood and lymphatic vessels undergo spontaneous rhythmical constrictions. Such activity is an intrinsic property of the smooth muscle in the walls of these vessels and is induced or enhanced by a wide range of activators including pressure-induced distension and sympathetic neurotransmitters in both blood vessels and lymphatic vessels. This review considers present understanding of vasomotion.
Abstract: Arterioles typically exist in a state of partial constriction that is related to the level of intraluminal pressure. This vasomotor response is a function of the vascular smooth muscle and occurs independently of neurohumoral and endothelial input. The physiological relevance of myogenic constriction relates to the setting of peripheral resistance, provision of a level of tone that vasodilators can access, and a contribution to control of capillary pressure. Despite its importance in the regulation of microvascular haemodynamics the exact cellular mechanisms linking intraluminal pressure to myogenic constriction remain uncertain. Studies using isolated, cannulated arteriole techniques, and freshly dispersed smooth muscle…cells, have shown that increased intraluminal pressure/cell stretch leads to smooth muscle cell membrane depolarisation, the opening of L-type voltage-gated Ca2+ channels (VGCC), Ca2+ -dependent activation of myosin light chain kinase and actomyosin-based contraction. Questions remain as to how the initial stimulus is detected and how these events lead to membrane depolarisation. A candidate pathway for the mechanosensory events involves the link between extracellular matrix proteins, cell surface integrins and the subsequent activation of intracellular signalling events. Membrane depolarisation may occur through the involvement of various ion channels, including non-selective cation channels (possibly themselves mechanosensitive) that predominantly pass Na+ from the extracellular space. Evidence suggests that this may involve TRP-like channels, possibly TRPM4 or TRPC6 isoforms that are modulated by diacylglycerol and protein kinase C. In addition, the exact roles played by various Ca2+ pools, including those occurring in spatially-restricted domains, and Ca2+ sensitisation, remain uncertain despite the clearly important role of VGCC. Similarly, while a change in intraluminal pressure is associated with the generation of a number of second messengers and the activation of various protein kinases, their roles in myogenic contraction versus long-term adaptive responses, such as tissue remodelling, are still to be defined.