Clinical Hemorheology and Microcirculation - Volume 10, issue 6

Article Type: Editorial

DOI: 10.3233/CH-1990-10617

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. I-III, 1990

Authors: Witte, Siegfried | Copley, Alfred L.

Article Type: Editorial

DOI: 10.3233/CH-1990-10601

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 569-570, 1990

Authors: Witte, Siegfried | Copley, Alfred L.

Article Type: Obituary

DOI: 10.3233/CH-1990-10602

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 571-572, 1990

Authors: Ehrly, Albrecht M.

Article Type: Other

DOI: 10.3233/CH-1990-10603

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 573-576, 1990

Authors: Stoltz, Jean-François

Article Type: Other

DOI: 10.3233/CH-1990-10604

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 577-579, 1990

Authors: Di Perri, Tullio

Article Type: Other

DOI: 10.3233/CH-1990-10605

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 581-595, 1990

Authors: Copley, A.L.

Article Type: Introduction

DOI: 10.3233/CH-1990-10606

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 597-599, 1990

Authors: Neumann, F.-J. | Tillmanns, H. | Kübler, W.

Article Type: Research Article

Abstract: The role of blood fluidity in acute coronary syndromes is still unclear. Various studies have revealed hemorheological abnormalities in unstable angina and myocardial infarction. These hemorheological abnormalities are basically independent of risk factor profile and extent of coronary artery lesions. In unstable angina they are related to the risk of myocardial infarction. This suggests that the hemorheological abnormalities have some link to the pathogenesis of the disease. Due to alterations of the atherosclerotic plaque, acute coronary syndromes are characterized by continuous or intermittent impairment of flow. This leads to an intensive interaction of platelets and white blood cells with the …vessel wall causing release of interleukins 1 and 6. The resulting expression of acute phase reactants in hepatocytes induces an increase in plasma viscosity and red cell aggregation. Experimental evidence suggests that hemorheological abnormalities may in turn impede nutritional coronary flow. In addition, the increase in red cell aggregation promotes the interaction of other blood formed elements with the vessel wall, which is the prime event of ischemic microvascular injury. Therefore, hemorheological abnormalities in acute coronary syndromes may represent both, cause and consequence of the disease. Show more

Keywords: Erythrocyte aggregation, blood viscosity, acute coronary syndromes, acute phase response, microcirculation

DOI: 10.3233/CH-1990-10607

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 601-611, 1990

Authors: Ehrly, A.M.

Article Type: Other

DOI: 10.3233/CH-1990-10608

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 613-620, 1990

Authors: Copley, A.L.

Article Type: Other

DOI: 10.3233/CH-1990-10609

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 621-623, 1990

Authors: Ehrly, A.M.

Article Type: Research Article

Keywords: In vivo-ridification of erythrocytes, microcirculation, hemorheology

DOI: 10.3233/CH-1990-10610

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 625-635, 1990

Authors: Heini, H. | Pfitzner, D. | Keuchel, M. | Ebel, H. | Lange, H. | Wichert, P.v.

Article Type: Research Article

Abstract: We compared the effect of a constant versus a decreasing ultrafiltration rate during hemodialysis on plasma viscosity, erythrocyte aggregation (hematocrit adjusted to 40%) and blood viscosity (hematocrit 40%; shear rates 23.04, 46.08, 115.2 and 230.4/″) in 5 woman and 10 men with chronic renal failure due to different origins, mean age 67.3 ± 6.7 years. Measurements were done before and after dialysis. The regimen with a constant ultrafiltration rate increased plasma viscosity (1.36 ± 0.09 to 1.48 ± 0.16 cPs, P < 0.01) and blood viscosity at high shear (230.4/″; 3.51 ± 0.34 to 3.91 ± 0.73 cPs, p < …0.05), the other parameters remained unchanged. There was a good correlation to the change in protein concentration before and after dialysis due to hemoconcentration (6.61 ± 0.54 to 7.51 ± 1.02 mg%, r = 0.85, p < 0.01). The regimen with a decreasing ultrafiltration rate caused no significant change in the rheological parameters. The weight loss was comparable in both regimens. We conclude that a decreasing ultrafiltration rate during hemodialysis is associated with less disturbances of rheology. Show more

Keywords: hemodialysis, blood rheology, plasma rheology

DOI: 10.3233/CH-1990-10611

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 637-644, 1990

Authors: Baumler, H. | Distler, B. | Scherf, H.-P. | Mockel, C. | Miller, H. | Lerche, D. | Papies, B.

Article Type: Research Article

Abstract: The possible influence of dialysis on the metabolism of reactive oxygen species as well as the flow properties of blood were investigated. 22 patients suffering from chronical renal failure were hemodialysed every second day. 11 of them were additional treated with ultraviolet irradiated own blood. The concentration of thiobarbituric acid reactive substances (TBARS) was normal (3.6±0.8 nmol) before hemodialysis and rose during hemodialysis up to 4.6±1.0 nmol). This increase of TBARS was no longer seen in the uv treated patients. The parameters of RBC aggregation were neither significantly different in the two patient groups before the treatment nor different in …comparison with healthy persons. The orientability of RBC of the patient groups was significantly reduced in comparison with that of the healthy group at the beginning of investigation and was significantly improved after uv treatment. The retransfusion of uv irradiated own blood seems to result in a decreased oxidative stress. Show more

Keywords: red blood cell, TBARS, lipid peroxiclation, oxygen radicals, RBC aggregation, RBC deformability

DOI: 10.3233/CH-1990-10612

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 645-652, 1990

Authors: Paulitschke, M. | Meier, W. | Lerche, D. | Zoellner, K. | Schmidt, G.

Article Type: Research Article

Abstract: The deformability of RBC in uremic hemodialysed children was determined by two different micropipette techniques (apparent elastic shear modulus of RBC membrane µ; entry time te and amplitude A) in dependence on the period of rhEPO administration. At the outset, mean hematocrit of the 10 children enclosed in the study was 0.20 +/− 0.02, mean predialysis levels of serum creatinine and urea nitrogen were (919 +/− 163)µMol/l and (24.3 +/− 3.0)mMol/l, respectively. Dialysis was performed with hollow fiber dialyzer three times a week for 4 hours each. Mean µ, te and A in children with end-stage renal disease …were found to be elevated by 126, 54 and 65 %, respectively, above corresponding mean values of the healthy reference group. Under the therapy with rhEPO mean values of µ, te and A were already significantly decreased by 67, 35 and 34 %, respectively, within the correction period (rhEPO dose: 100 IU/kg/week). In the maintenance period of rhEPO therapy (Hct = 0.30 +/− 0.03) the mean values of deformability parameters reached those of the healthy reference group. Mean cell volume of uremic erythrocytes rose significantly under rhEPO administration. This study showed that under rhEPO therapy apart from the desired correction of anemia of end-stage renal disease the impaired rheological properties of uremic RBC will also be normalised. This findings underline that the impaired RBC deformability in hemodialysed uremic patients cannot be attributed to “uremic toxines” alone. Show more

Keywords: uremia, erythropoietin, RBC membrane, shear elastic modulus, deformability/passage analyzer, cell volume

DOI: 10.3233/CH-1990-10613

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 653-664, 1990

Authors: Mineshita, Takeshi

Article Type: Abstract

DOI: 10.3233/CH-1990-10614

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 665-670, 1990

Article Type: Announcement

DOI: 10.3233/CH-1990-10615

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 671-672, 1990

Article Type: Other

DOI: 10.3233/CH-1990-10616

Citation: Clinical Hemorheology and Microcirculation, vol. 10, no. 6, pp. 673-675, 1990