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: Activated protein C (APC) is a serine protease that plays a central role in physiological anticoagulation, and has more recently been shown to be a potent anti-inflammatory mediator. We show here that APC upregulates the angiogenic promoters, vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8) or matrix metalloproteinase-2 (MMP-2) in cultured human skin fibroblasts (HF), keratinocytes (HK) or umbilical vein endothelial cells (HUVE). In the chick embryo chorio-allantoic membrane assay, APC promoted angiogenesis. In a full-thickness rat skin healing model, a single topical application of APC enhanced wound healing compared to saline control. In summary, our results…demonstrate that APC promotes cutaneous wound healing at least partly by stimulation of angiogenesis.
Abstract: Generation of reactive oxygen species (ROS) and their detrimental effects on the brain after transient ischemia are widely recognized. We studied ROS production from mitochondria in human brain microvessel endothelial cells (HBEC) under chemical hypoxia. HBEC in confluent conditions were incubated for 30 min with 10 μM 5-(and-6)-carboxy-2′,7′-dichlorodihydrofluorescein (DCF) diacetate, which was hydrolyzed and trapped inside the cells. ROS were measured with a fluorescent microscope, a CCD camera and an image analyzing system. Injury to mitochondrial respiratory chain was induced either with rotenone (an inhibitor of mitochondrial complex I) or with m-chlorocarbonyl cyanide phenylhydrazone (CCCP) (an uncoupler of ATP synthetase).…Shortly after application of 10 μM rotenone, fluorescent intensity started to increase and the gradual increase continued for 10 min. Similarly, CCCP (10, 50 and 100 μM) dose-dependently increased the fluorescent intensity (p<0.01). Edaravone, a free radical scavenger widely used for treatment of cerebral infarction in Japan, at 100 μM successfully suppressed this ROS production (p<0.05). These data show that chemical hypoxia with normal concentration of oxygen in the medium induced free radicals generation in HBEC. Importance of endothelial mitochondria as a source of free radicals after reperfusion is suggested.
Keywords: Human brain, microvessel, endothelial cell, reactive oxygen species (ROS), dichlorodihydrofluorescein
Abstract: Rho-kinase modulates calcium sensitivity of the myosin light chain in smooth muscle cells and has been implicated as playing a pathogenetic role in cardiovascular disorders. This paper was aimed to determine whether hydroxyfasudil (a specific Rho-kinase inhibitor) exerts cardioprotective effect on coronary ischemia–reperfusion (I/R) injury, and if so, whether NO is involved. Canine subepicardial small arteries (diameter≥100 μm) and arterioles (diameter<100 μm) were observed by a CCD intravital microscope during coronary I/R. Coronary vascular responses to endothelium-dependent (acetylcholine) and -independent (papaverine) vasodilators were examined after I/R under three conditions: control, preconditioning, and hydroxyfasudil. Coronary I/R significantly impaired coronary vasodilation to…acetylcholine, whereas hydroxyfasudil completely preserved the responses, as did preconditioning. Hydroxyfasudil also significantly reduced myocardial infarct size. These results indicated that hydroxyfasudil exerts cardioprotective effects on coronary I/R injury in vivo, for which NO-mediated mechanism may be involved.
Abstract: Connective tissue growth factor (CTGF) is a 38-kDa cysteine-rich protein and an important regulator of angiogenesis. In order to study the role CTGF gene playing in angiogenesis, the eukaryotic expression vector of CTGF gene was constructed in this study, and the role of endogenous CTGF on migration of human umbilical vein endothelial cell (HUVECs) was investigated. According to human CTGF cDNA sequence, a pair of specific primers containing digestion sites of Xba I and Hind III on the 5′ end respectively were designed. Reverse transcript polymerase chain reaction (RT-PCR) was used to amplify CTGF cDNA from HUVECs. The eukaryotic expression…vector pcDNA3.1(−)/CTGF containing the entire coding region was constructed successfully. Compared with CTGF sequence of GenBank, DNA sequence analysis showed that this reformed plasmid contained the same full length of CTGF cDNA. The results of Western blotting demonstrated that CTGF was over-expressed at 48 h after transfection. Migration of HUVECs transfected with CTGF vector increased significantly compared with those transfected with vector control. In conclusion, the eukaryotic expression vector pcDNA3.1(−)/CTGF was constructed successfully and the endogenous CTGF promoted the migration of HUVECs. This study lays a foundation for further study on the role CTGF gene playing in angiogenesis.
Abstract: To clarify the microvascular changes and the effector sites of lansoprazole during the formation of colitis, the dextran sulfate sodium (DSS)-induced colitis was induced by the oral administration for 3 and 7 days. The alteration of the microvascular permeability was estimated by the intraaortic infusion of FITC-dextran. The effector sites of 3 H-lansoprazole were examined by the intraaortic infusion of the radiolabelled compound and the autoradiographic procedure of water-soluble compounds. As a result, marked increase of the microvascular permeability was detected three days after DSS treatment near the inflammatory cells in the tip portion of the colonic mucosa. 3 H-lansoprazole…in the control rat colon was localized in the goblet cells, while in DSS-treated rats, 3 H-lansoprazole was accumulated in the cytoplasm of the mesenchymal cells, and most of them coincided with polymorphonuclear leucocytes and macrophages.
Abstract: Hypoxia is generally considered to represent a fundamental stimulus for angiogenesis. Most angiogenic factors were up-regulated by hypoxia, but as a strong angiogenic and antiapoptotic factor, hepatocyte growth factor (HGF) was down-regulated by hypoxia. In order to investigate whether hypoxia inducible factor 1a (HIF-1α) participate in the transcriptional regulation of HGF under hypoxia, rat cardiac myocytes were treated with cobalt chloride (CoCl2 ), the specific inducer of HIF-1α, for different times, and total RNA and protein were isolated to perform RT-PCR and Western blot. Results show the expression of HGF mRNA in cardiac myocytes decreased distinctively after treating with CoCl2…for 12 hours. However, at the same time, the expression of HIF-1α protein was up-regulated. HIF-1α may be participate in the transcriptional regulation of HGF indirectly.
Abstract: Although microvascular complications are frequent in diabetes, the pathogenesis underlying these morbidities remains unclear. Chronic inflammation appears to play a role both in the development of vascular dysfunction and diabetes. Evaluation of microvascular status in the prediabetic stages would provide a better insight into the natural progression of the disease, both from the vascular and metabolic perspective. Microvascular function was assessed in sixty rhesus monkeys using laser Doppler fluximetry. These included monkeys who had been calorie-restricted (CR); normal non-diabetic ad libitum fed (N) monkeys; Prediabetic (PreDM) monkeys with either impaired fasting glycemia, glucose intolerance or insulin resistance; and overtly diabetic…monkeys (DM) with fasting glucose levels above 126 mg/dl. Body weight, per cent body fat, fasting glucose and insulin levels, glucose disposal rate during an intravenous glucose tolerance test (Kglucose ), and insulin sensitivity (M-rate) as assessed by the euglycemic, hyperinsulinemic clamp procedure were measured. Routine clinical chemistry and hematology were also performed. Our results show that in prediabetes, dermal microvascular flow is characterized by an increase in response to thermogenic provocation. We further show that this paradoxical increase is significantly and highly correlated with circulating high sensitivity CRP levels. The study demonstrates that both mild chronic inflammation and elevated skin microvascular perfusion precede overt diabetes.
Abstract: This study was aimed to investigate chronic changes of the iris microvasculature in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced in male Wistar-Furth rats by intravenous injection of STZ (55 mg/kg.bw). The rats were divided into control (CON) and diabetic (STZ) groups. The experiments were performed at 8, 12, 24 and 36 weeks after the injection of STZ. The iris microcirculation was visualized under a fluorescence videomicroscope. Intraluminal diameters of microvessels were measured based on the FITC-dextran images. Leukocyte adhesion to the microvascular endothelium was evaluated by counting leukocytes (labeled with rhodamine 6G). The iris blood perfusion was measured using…laser Doppler flowmetry. Tissue lipid peroxidation of the eye was evaluated. The results demonstrated that the lipid peroxidation increased significantly after the injection of STZ. Both the diameters of arterioles (or precapillaries) and the iris blood perfusion decreased significantly in STZ rats, compared to the control levels. Adherent leukocytes increased significantly at 8, 12, 24 and 36 week after the injection of STZ, compared with the control levels. This indicates that the increased in oxygen-derived free radicals may be a major contributor for iris vascular endothelial dysfunction in diabetes mellitus, including leukocyte adhesion and reducing the arteriolar diameter. The present model may be useful for assessing long-term effects of therapeutic agents on diabetic retinopathy.
Abstract: The purpose of this study was to determine the role of exercise training on blood flow in diabetic dental pulp. Male Spraque-Dawley rats were divided into three groups of control (CON), diabetes (STZ), and diabetes with exercise-trained (STZ + Ex) groups. Diabetes was induced by intravenous injection of streptozotocin (STZ; 55 mg/kg.bw). The exercise training protocol consisted of treadmill running, 5 times/week with the velocity of 13–15 m/min for 30 min. At 12 weeks (wks) and 24 wks after the STZ injection, the laser Doppler flowmeter (Model ALF 21, USA) was used to measure pulpal blood flow (PBF) while the…animals were anesthetized with sodium pentobarbital (50 mg/kg.bw). The results showed that STZ rats developed hyperglycemia, hypertriglyceridemia, higher mean arterial blood pressure, higher heart weight, body weight loss, and lower of PBF in the intact right lower incisor. Exercise training has beneficial effect on physiological characteristics of diabetic condition including triglyceride level, mean arterial blood pressure, heart rate, and heart weight. Interestingly, reduction of the PBF was restored in STZ + Ex rats. In conclusion, our observations indicate that exercise training can prevent the reduction in PBF of STZ-induced diabetic rats.
Abstract: The involvement of plasma nitric oxide metabolites (NOx ) in hypertension was examined in stroke-resistant spontaneously hypertensive rats during the development of hypertension. Continuous application of a static magnetic field (SMF; a maximum magnetic flux density of 180 millitesla, a peak magnetic gradient of 133 millitesla/mm) to the left carotid sinus baroreceptors of rats was carried out for 6 weeks using a disc-shaped magnetic implant (4.4 mm in diameter, 2.2 mm in height). An L-type voltage-gated Ca2+ channel blocker, nicardipine (2 mg/kg) was administered intraperitoneally three times a week for 6 weeks, and then 15 min after each injection,…mean arterial blood pressure (MAP), heart rate (HR), skin blood flow (SBF), skin blood velocity (SBV) and plasma NOx were monitored. The nicardipine significantly decreased MAP, and increased HR, SBF and SBV in the nicardipine-treated rats compared with the control rats (p<0.001) without changing plasma NOx levels. The SMF exposure alone significantly suppressed or retarded the development of hypertension in SMF-exposed rats compared with the control rats (p<0.05). The SMF significantly promoted the nicardipine-induced MAP decrease (p<0.001) and induced a significant increase in plasma NOx levels (p<0.01) in SMF-exposed, nicardipine-treated rats compared with the unexposed, nicardipine-treated rats. The SMF did not significantly induce any changes in the SBF and SBV in nicardipine-treated nor untreated rats. These results suggest that the SMF may enhance nicardipine-induced hypotension by more effectively antagonizing the Ca2+ influx through the Ca2+ channels compared with the nicardipine treatment alone. In addition, the enhanced antihypertensive effects of the SMF on the nicardipine-treated rats might be, at least in part, related to the increased NOx , primarily due to the upregulation of inducible nitric oxide synthase.