Clinical Hemorheology and Microcirculation - Volume 32, issue 3
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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: Microcirculatory alterations would explain focal lesions found in Chagas' cardiomyopathy. Trypanosoma cruzi (T. cruzi) infection induces host blood properties modifications and defensive responses capable of producing blood hyperviscosity, an ischemic risk factor able to affect microvascular blood flow. We studied whole blood viscosity (ηb ) and plasmatic and cellular factors influencing it in rats, 7 and 14 days after experimental infection with T. cruzi. Increased plasma viscosity (ηp ) was found in infected versus control rats and it was correlated with high blood parasite levels at 7 days and enhanced γ‐globulin fraction concentration at 14 days. The hematocrit, mean corpuscular…volume (MCV) and ηb were higher in 14 days infected rats vs. 7 days and control animals. Also, electron microscopy observation showed morphological changes in red blood cells (RBC) at 7 and 14 days post‐infection, with increased proportion of echinocyte and stomatocyte shapes transformation. In our rat model of Chagas' disease, BPL, increased plasmatic protein concentration, enhanced MCV and RBC shapes transformation would determine blood hyperviscosity, cause of microvascular blood flow abnormalities.
Abstract: Hemorheological parameters were determined in 45 pairs of mothers with severe preeclampsia and their newborns in comparison with 45 women with uncomplicated pregnancies and their newborns. In both groups we investigated red cell deformability, the plasma viscosity, the red cell aggregation (during stasis and low flow), the macromolecules fibrinogen and factor VIIIR:Ag (VWF), and the blood count parameters hemoglobin, hematocrit, white cells, platelets, reticulocytes, MCV, MCHC. Cholesterol and triglycerides were correlated to the parameter of red cell deformability measured as red cell elongation. We found a significant lower plasma viscosity, red cell aggregation, fibrinogen, cholesterol, triglycerides and VWF in cord…blood with a close association between plasma viscosity and fibrinogen (r=0.56, p=0.001). The red cell deformability measured as red cell elongation was statistically higher in the cord blood compared to the mothers and associated with a higher MCV. In contrast the MCHC values remained unchanged. Hematocrit and hemoglobin in the cord blood were higher than in the mothers. The incidence of fetal hyperviscosity‐polycytemia syndrome in women with severe preeclampsia was between 4.7% and 4.9%. An elevated red cell aggregation was found in 2.8% (stasis) and 4.8% (low flow state), respectively. We conclude that in fetal blood the higher hematocrit and the presence of larger red cells do not cause impaired fetal hemorheology.
Abstract: The study provides information on the blood fluidity in healthy, juvenile sheep and rabbits during growth (n=18), and shows also data from fetal rabbits and cats. In the fetal rabbit (n=3) and cat (n=2), whole blood viscosity (WBV; LS30, Contraves, Switzerland) and plasma viscosity (PV; OCR‐D, Paar, Austria) was low (WBV (0.7 s−1 ): rabbit: 3.28/3.00/2.44; cat: 7.87/10.88; WBV (94 s−1 ): rabbit: 2.57/2.48/2.39; cat: 2.75/3.73 mPa s) (PV: rabbit: 1.10/1.10/1.05; cat: 1.27/1.39 mPa s), which was associated with a low plasma protein concentration and a low erythrocyte count despite a high erythrocyte volume. After parturition, blood viscosity increased in rabbits in…parallel with hematocrit, while MCV decreased (WBV (0.7 s−1 ): 9.28 (8.07/10.88); WBV (94 s−1 ): 3.67 (3.62/3.82); PV: 1.15 (1.15/1.25) mPa s). In contrast, in the sheep, whole blood and plasma viscosity decreased after delivery (WBV (0.7 s−1 ): 1.31 (0.94/1.88); WBV (94 s−1 ): 2.45 (2.43/2.85) PV: 1.24 (1.23/1.29) mPa s). Hematocrit and MCV decreased, while erythrocyte count increased under these circumstances. In summary, whole blood viscosity was similar among fetal sheep, rabbits, and cats and is diminished compared to adult individuals to guarantee an optimal oxygen supply during a period of life in which the oxygen maintainance of the child depends on the health and the environment of the mother. However, during growth, blood viscosity rose in rabbits, while it continously decreased in the sheep. At an unknown time point this fall in blood viscosity in lambs must reverse, since adult sheep again show a higher blood viscosity than juvenile lambs at the age of 2 months.
Abstract: Capillary angiogenesis and remodeling induced by arteriovenous (AV) shunting in rat hind limb was investigated by evaluating changes in capillary density and diameter in the skeletal muscle subject to retrograde flow and high pressure. Wistar rats were used, and an AV anastomosis was created in the hind limb. Two weeks after AV shunting, the microvasculature in the limb was visualized by GS‐lectine, and the samples were observed using confocal laser microscopy. The capillary density were increased by approximately 150% for small vessels (<13 μm in diameter) under retrograde flow condition, but no change appeared for large vessels (>13 μm in…diameter). The capillary diameters were not significantly different between control and chronic condition. In conclusion, retrograde flow produced by AV shunting increased capillary density but it did not change the capillary diameter significantly.
Abstract: This experiment was designed to study the therapeutic mechanisms of Angelica on the focal cerebral ischemia injury of the rat. The ischemic area was determined by TTC stain. And terminal deoxynucleotidyl transferase (TDT) mediated DUTP‐biotin nick end labeling (TUNEL) method was applied to detect neuronal apoptosis. The expressions of Bcl‐2 and Bax proteins were observed by immunohistochemical staining methods. Results show that the treatment with angelica reduced the volume of cerebral infarction (p<0.05), and that the number of neuronal apoptosis cells decreased significantly (p<0.01). Also the expression level of Bax protein decreased (p<0.01). These results suggest that Angelica can reduce…the number of apoptosis cells by decreasing the expression of Bax protein. This is maybe one of the mechanisms of the therapeutic effect of Angelica on focal cerebral ischemia injury.
Abstract: The protective effects of exercise training on the diabetic‐induced endothelial cell (EC) dysfunction were determined using intravital fluorescent microscopy. Male Spraque‐Dawley rats were divided into three groups of control (Con), diabetes (DM), and diabetes with exercise – training (DM+Ex). Diabetes was induced by single intravenous injection of streptozotocin (STZ; 50 mg/kg BW). The exercise training protocol consisted of treadmill running, 5 times/week with the velocity of 13–15 m/min, 30 min/day periods for 12 and 24 weeks (wks). 24 wks after the STZ injection, blood glucose (BG), glycosylated hemoglobin (HbA1C ), mean arterial blood pressure (MAP) and heart weight (HW) were…significantly higher in DM rats (p<0.001). However, DM+Ex rats had reduced the abnormalities of MAP (p<0.01) and HW (p<0.05) compared with DM rats. Furthermore, there was a significant decrease in heart rate (HR) of DM+Ex rats (p<0.05) relative to Con rats. To examine the influence of exercise training on EC dysfunction, leukocyte–EC interactions in mesenteric venules and vascular reactivity responses to vasodilators in mesenteric arterioles were monitored by using intravital fluorescence microscopy. The diabetic state enhanced leukocyte adhesion in mesenteric postcapillary venules (p<0.001). Moreover, an impaired vasodilatory response to the EC‐dependent vasodilator, acetylcholine (Ach), not to sodium nitroprusside (SNP), was found in 12‐ and 24‐wk diabetic rats (p<0.01). The leukocyte adhesion and the impairment of EC‐dependent vasodilation to Ach were attenuated by exercise training (p<0.05). In addition, exercise training was also shown to have favorable preventive effects on hyperglycemia induced oxidative stress, as lower malondialdehyde (MDA) levels were observed from both groups of 12 and 24 weeks DM+Ex compared with DM (p<0.01). In conclusion, our findings indicate that the endothelial dysfunction of diabetic rats could be characterized by increased leukocyte adhesion and impaired endothelium‐dependent relaxation. Regular low intensity exercise training could improve both indices of endothelial dysfunction through amelioration of diabetic‐induced oxidant/antioxidant levels. These findings support the notion that regular exercise training could be a fundamental form of therapy in preventing diabetic cardiovascular complications potentiated by endothelial dysfunction.
Abstract: The influence of contrast media on blood viscosity, erythrocyte morphology and platelet function was studied. In vitro blood was incubated with iopromide (Ultravist® ), ioxaglate (Hexabrix® ) or gadolinium‐DOTA (Dotarem® ). Plasma viscosity and whole blood viscosity were measured and the mean erythrocyte volume and morphology were assessed. Platelet aggregation was measured with a PFA‐100® instrument. In an ex vivo study on patients receiving these contrast media the same measurements as described above were done. All contrast media increased blood viscosity at high shear rate in a dose dependent manner (e.g. with ioxaglate: from 4.9±0.2 mPa.s to 8.6±0.5 mPa.s…at 160 mg I/ml), decreased low shear viscosity (for ioxaglate: from 44.9±2.5 to 27.7±4.8 mPa.s), increased plasma viscosity (ioxaglate: from 1.2±0.1 to 2.8±1.3 mPa.s), decreased the mean erythrocytic volume (ioxaglate: from 89.7±1.4 to 79.7±2.0 fl) and decreased platelet aggregation. Iopromide induced an echinocytic shape transformation of erythrocytes. Ex vivo a decreased hematocrit and a consecutively decreased whole blood viscosity were found with iopromide and ioxaglate. We conclude that contrast media influenced blood rheology, erythrocytes and platelet aggregation in vitro and ex vivo.