Clinical Hemorheology and Microcirculation - Volume 24, issue 4
Purchase individual online access for 1 year to this journal.
Price: EUR 185.00
Impact Factor 2016: 1.815
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: Fatty liver disease (FLD) characterised by a high plasma levels of lipoproteins and remnant‐like lipoproteins (RLP) is a risk factor for impaired microvascular blood flow, endothelial cell dysfunction and atherosclerosis. Using an immunoseparation technique with a gel mixture containing human monoclonal antibodies to apo A‐I and apo B‐100, we separated and measured RLP cholesterol (RLP‐C) levels which reflect RLP in patients with FLD (n=20). Whole blood transit time (TT) was determined by a microchannel method (MC‐FAN) which allows blood flow to be viewed via a microscope connected to an image display unit. RLP‐C levels were higher (P<0.01) in FLD, 15.6…± 1.0 mg/dl compared with 4.8 ± 0.5 mg/dl for controls (n=20). Similarly, TT was longer (P<0.01) in FLD, 284.5 ± 26.1 sec/100 μl compared with 82.8 ± 1.0 sec/100 μl for controls. Since the liver is a major site for RLP formation and degradation, it is affected to a greater extent in patients with FLD. It is likely that high levels of RLP can impair microvascular perfusion in the liver tissue and contribute to the development and progression of FLD.
Abstract: The present study examined the influence of ingesting a moderate dose of alcohol on the main determinants of blood rheology namely: plasma viscosity, plasma fibrinogen concentration, plasma total protein concentration, and haematocrit. Eleven moderately active young men were studied immediately after a standardised cycle ergometer test and during the 24 h period of recovery. Alcohol (0.7 g/kg body mass) was given 1 h after exercise on one test occasion, while an equal volume of alcohol‐free solution was administered on the other. Venous blood samples were obtained at baseline, post exercise, and at 1, 5, and 22 h post alcohol ingestion.…A significant reduction in plasma volume was observed immediately after exercise, but this decrease was restored 1‐h post drink ingestion. Blood alcohol level increased significantly 1 h after the ingestion of alcohol, but decreased and returned to the resting baseline level at 5 h during recovery. Exercise induced significant changes (P<0.05) in blood rheology as manifested by a significant increase (P<0.05) in plasma viscosity and plasma fibrinogen. Parallel increase (P<0.05) in haematocrit and total protein was also observed after exercise. The increase in these rheological variables immediately after exercise was mainly due to exercise‐induced plasma volume loss. During recovery, while the increase in haematocrit post‐exercise returned to the baseline level in both control and alcohol trials, plasma viscosity and plasma fibrinogen remained significantly high during recovery in the alcohol trial compared with control condition. It is concluded that exercise induces significant changes in the main determinants of blood rheology and the consumption of alcohol after physical exercise delays the normal return of plasma viscosity, plasma fibrinogen to the resting baseline levels during recovery. Although the mechanism responsible for these findings is not, as yet known, it might be linked with alcohol induce dehydration.
Abstract: Ischemia leads to profound endothelin‐related constriction of the hepatic microcirculation with resulting disturbances in blood and oxygen supply. The aim of the study was to modulate hepatic microvascular diameters by blocking endothelin receptors with bosentan, and also to find the best possible vessel width (as produced by bosentan) for minimizing ischemia/reperfusion injury. Methods: In an in vivo rat model hepatic ischemia was induced for 30 minutes by crossclamping the hepatoduodenal ligament. The endothelin receptor antagonist (ERA) bosentan was administered before ischemia in stepwise dosages of 0.1, 1.0 and 10 mg/kg bw i.v. and 10 mg/kg bw intraportally (i.p.). Vasoactive…effect was assessed by in vivo microscopy. The influence on hepatic oxygen supply and hepatocellular function was evaluated by measuring local tissue pO2 and AST levels. Results: Because of ischemia sinusoidal diameters were reduced to 76.3 ± 7.4% compared with values found in sham‐operated animals. After administration of 0.1 mg/kg ERA (bosentan) the sinusoids remained constricted (89.7 ± 9.9%). Blocking endothelin receptors with 1 mg/kg bosentan avoided sinusoidal constriction (99.0 ± 8.8%, p<0.05) and led to the most effective reduction of AST level peak after 6 h of reperfusion (244.0 ± 34.2 U/l vs 422.9 ± 163.3 U/l in untreated ischemia). 10 mg/kg i.v. caused an increase in sinusoidal diameter to 109.1 ± 6.4% and 10 mg/kg intraportally to 136.8 ± 19.3% and even an increase in AST levels (618.9 ± 209.3 U/l). Hepatic ischemia led to a significant decrease of local tissue pO2 after reperfusion (9.4 ± 1.2 mm Hg; p<0.05 vs sham: 16.8 ± 1.8 mm Hg). The greatest improvement in postischemic oxygen supply was found in the 1.0 mg/kg group (12.9 ± 1.0 mm Hg; p< 0.05 vs ischemia). Venular diameter changed almost to the same extent as sinusoidal diameter. Perfusion rate was significantly increased and sticking of leukocytes in sinusoids and venules was reduced after doses of 1 and 10 mg/kg bw bosentan i.v. (p<0.05). Implications: In this model we were able to regulate the diameters of sinusoids and postsinusoidal venules incrementally. We conclude that the avoidance of constriction, without excessive vasodilatation gives increased perfusion rates with improved hepatic oxygen supply and hepatocellular function.
Abstract: The effects of plasma triglycerides level on human red blood cells (RBCs) indices, hematological parameters, RBCs aggregation velocity and whole blood viscosity were studied at 2 hours after high‐fat or low‐fat meal. Proteins, triglycerides and cholesterol levels of plasma were analysed. The RBCs rouleaux formation rate was measured in 70% autologous plasma (with 30% phosphate‐buffered saline, PBS) or 1 g/dl dextran T70 solution (with 4 g/dl bovine serum albumin) in PBS, using a low‐shear rheoscope. The results were grouped according to triglycerides content in plasma. No significant difference in whole blood viscosity, hematological parameters, RBC indices, protein and cholesterol content…was observed between high‐fat and low‐fat blood samples. There was a significant increase in rouleaux formation rate of samples with high triglyceride levels, when measured in 70% autologous plasma, but it was not significant in dextran T70 containing medium. In conclusion, the results obtained suggest that alteration of plasma lipid levels as well as possible changes in the cell membrane lipid composition lead to enhanced RBC aggregation.
Keywords: Red blood cells, red blood cell aggregation, plasma triglycerides