Enhancement of Heat Transfer in Red Cell Suspensions In Vitro Experiments

1989 ◽  
Vol 111 (2) ◽  
pp. 152-156 ◽  
Author(s):  
R. T. Carr ◽  
N. R. Tiruvaloor
Keyword(s):  
Heat Transfer ◽  
Blood Cell ◽  
Cell Suspensions ◽  
Red Cells ◽  
Red Cell ◽  
In Vitro Experiments ◽  
Enhancement Of Heat Transfer ◽  
Heating And Cooling ◽  
Sheared Suspensions

New data on laminar heat convection with red cell suspensions have been gathered for both heating and cooling. When compared to data for the suspending medium alone, it is apparent that the red cells enhance laminar heat transfer when Pe > 4. This is probably due to particle movements. These new data disagree with earlier studies which indicated no enhancement of heat transfer for blood cell suspensions. The data do agree with previous correlations for enhanced thermal transport in sheared suspensions.

Mechanism of hemolysis after intravenous glycerol administration

1960 ◽  
Vol 198 (4) ◽  
pp. 895-898 ◽  
Author(s):  
Gabriel G. Pinter ◽  
D. B. Zilversmit
Keyword(s):  
Intravenous Injection ◽  
Rapid Decrease ◽  
Cell Suspensions ◽  
Glycerol Concentration ◽  
Red Cell ◽  
In Vitro Experiments ◽  
Intravascular Hemolysis ◽  
Hemolytic Effect ◽  
Similar Solutions

Concentrated glycerol solutions in 0.9% saline, when administered intravenously to rabbits and rats, caused considerable intravascular hemolysis, but similar solutions given to dogs had no hemolytic effect. Perfusion of the partially isolated hind leg of the rabbit with Cr51-tagged and glycerol-containing red cell suspensions showed hemolysis of only those cells containing glycerol. This observation eliminates a hemolysin as the cause for the hemolysis. In vitro experiments showed that glycerol penetrates the erythrocytes of rats, rabbits and man quite rapidly, whereas the cells of dogs were penetrated at a much slower rate. It is suggested that the intravascular hemolysis caused by intravenous glycerol is produced by the rapid uptake of glycerol by the erythrocytes and a subsequent osmotic imbalance caused by the rapid decrease of glycerol concentration in the circulating plasma. It is proposed that this mechanism is a general one and explains, for example, the intravascular hemolysis caused by the intravenous injection of hyperosmotic urea dissolved in 0.9% saline.

Nitrite and Red Cell Function in Carp: Control Factors for Nitrite Entry, Membrane Potassium Ion Permeation, Oxygen Affinity and Methaemoglobin Formation

1990 ◽  
Vol 152 (1) ◽  
pp. 149-166 ◽  
Author(s):  
FRANK B. JENSEN
Keyword(s):  
Cell Function ◽  
Oxygen Affinity ◽  
Red Cells ◽  
Red Cell ◽  
In Vitro Experiments ◽  
K Uptake ◽  
The Mean ◽  
K Release

Red cell function was studied in carp by a combination of in vivo and in vitro experiments with nitrite as the perturbing agent. In vivo accumulation of nitrite caused a marked increase in the red cell methaemoglobin content, and reduced the mean cellular volume. The oxygen affinity of unoxidized haemoglobin was strongly decreased, partly as result of the elevated concentration of cellular nucleoside triphosphates and haemoglobin associated with red cell shrinkage. Red cell pH was unchanged compared to controls, but reduced when referred to constant extracellular pH and O2 saturation. The mean cellular K+ content decreased, reflecting a K+ loss from the red cells during their shrinkage. This K+ loss contributed significantly to the large plasma hyperkalaemia during nitrite exposure. In vitro experiments revealed that nitrite influx into deoxygenated red cells was much larger than into oxygenated red cells. Nitrite permeation of the red cell membrane was not inhibited by DIDS and did not change extracellular pH. Methaemoglobin (MetHb) formation was more pronounced in deoxygenated blood than in oxygenated blood, but quasi-steady states were reached, reflecting a balance between nitrite-induced MetHb formation and the action of MetHb reductase. Red cells incubated in the oxygenated state released K+, whereas a net K+ uptake occurred in deoxygenated cells. Nitrite did not change the K+ loss from oxygenated cells, but shifted the K+ uptake in deoxygenated cells to a pronounced K+ release by the time high MetHb levels were reached. Both types of red cell K+ release were inhibited by DIDS and appeared to occur via a route involving Band 3. The data are consistent with the hypothesis that a significant DIDS-sensitive K+ efflux from the red cells occurs whenever a large fraction of the haemoglobin molecules assumes an R-like quaternary structure.

Reduction of Prion Infectivity in Packed Red Cells by Separation of Whole Blood and Washing of the Red Cell Fraction.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2890-2890
Author(s):  
Rodrigo Morales ◽  
Kimberley A. Buytaert-Hoefen ◽  
Eric T. Hansen ◽  
Dennis Hlavinka ◽  
Raymond Goodrich ◽  
...  
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Whole Blood ◽  
Red Cells ◽  
Cell Fraction ◽  
Health Concern ◽  
Red Cell ◽  
New Variant

Abstract Although prion diseases are rare in humans, the established link between a new variant form of CJD (vCJD) and the consumption of cattle meat contaminated by BSE have raised concerns about a possible outbreak of a large epidemic in the human population. Over the past few years, BSE has become a significant health concern in several countries, and it now seems apparent that vCJD can also be iatrogenically transmitted from human to human by blood transfusion. Exacerbating this state of affairs is the lack of a reliable test to identify individuals incubating the disease during the long and silent period from the onset of infection to the appearance of clinical symptoms. The purpose of this research study was to evaluate the effectiveness of separation of whole blood and washing of the red cell fraction for the removal of infectious scrapie prion protein (PrPSc) from red blood cell (RBC) suspensions. Samples of human, whole blood were spiked with 5 × 106 LD50 263K PrPSc. Analysis of the treated sample supernatants by Western blot revealed that approximately >88% of the PrPSc was removed with the initial plasma expression and the equivalent of 6% was detected in a saline wash (300 mL; 0.9% saline). The final sample of RBCs revealed no detectable levels of PrPSc by Western blots. Further analysis of the treated RBCs using the PMCA assay indicated detectable amounts of PrPSc only after 2 consecutive amplification rounds. Semi-quantitative analysis of PMCA amplification enabled us to estimate that the treated RBCs contained less than 1 × 104 LD50 PrPSc. This corresponded to removal levels exceeding ≥99% of spiked material in whole blood. These in vitro estimations were confirmed by in vivo infectivity studies in a hamster model of disease transmission. Results from in vivo studies displayed significant differences in the incubation periods of the spiked blood inoculated hamsters (100.1 ± 1.7) versus washed RBCs (135.8 ± 6.7). Moreover, a substantial difference in the attack rate (6/15: 40% in washed RBC, versus 13/13: 100% in spiked blood) further indicated a substantial removal of infectious prions. Comparison of this data with results of animals inoculated with different dilutions of infectious material, indicated a >99.94% reduction of infectivity. Washed, packed human red cells produced by this procedure were able to be stored in standard additive solutions (AS-3) for 42 days while still meeting all in vitro blood bank standards for acceptable red cell quality. Conclusion This data suggests that separation of plasma coupled with a simple, low volume wash of red cells may represent an efficient method to remove prions from red blood cell fractions, thus reducing possible infectivity of these products.

scholarly journals Resistance of Reticulocytes and Young Erythrocytes to the Action of Specific Hemolytic Serum

Blood ◽  
1952 ◽  
Vol 7 (6) ◽  
pp. 602-606 ◽  
Author(s):  
W. O. CRUZ ◽  
P. C. JUNQUEIRA
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Normal Animal ◽  
Red Cells ◽  
Normal Adult ◽  
Severe Anemia ◽  
Red Cell ◽  
Photoelectric Method ◽  
The Relationship

Abstract A photoelectric method is used to determine the degree of hemolysis produced by specific hemolytic serum on erythrocytes of dogs, taking as a standard the amount required for 50 per cent hemolysis. The requirement of the normal dog red blood cell is 1.2 cu. ml. (±0.7 cu. ml.) of hemolytic serum, under the conditions described in the method. The red cells of dogs given a sufficient dose of acetylphenylhydrazine to produce a severe anemia, followed by an intense period of blood regeneration, required an amount of hemolytic serum about two to four times greater than in the normal animal (values from 3.0 to 4.8 cu. ml. of hemolytic serum are recorded). This result shows that the reticulocytes and young erythrocytes are much more resistant than the normal adult red cell to the action of hemolytic serum. It was possible by this technic to concentrate the reticulocytes in vitro, destroying selectively the adult erythrocytes of a sample of blood by an appropriate amount of specific hemolytic serum. The relationship between these results and the high reticulocytosis observed during crisis in hemolytic jaundice is discussed.

LACK OF EFFECT OF CORTICOSTEROIDS ON THE IN VIVO DISAPPEARANCE OF SULFHYDRYL-INHIBITED AND ANTIBODY-COATED ERYTHROCYTES

1964 ◽  
Vol 47 (3_Suppl) ◽  
pp. S28-S36
Author(s):  
Kailash N. Agarwal
Keyword(s):  
Red Cells ◽  
List Type ◽  
Red Cell

ABSTRACT Red cells were incubated in vitro with sulfhydryl inhibitors and Rhantibody with and without prior incubation with prednisolone-hemisuccinate. These erythrocytes were labelled with Cr51 and P32 and their disappearance in vivo after autotransfusion was measured. Prior incubation with prednisolone-hemisuccinate had no effect on the rate of red cell disappearance. The disappearance of the cells was shown to take place without appreciable intravascular destruction.

Cytogenetic, anatomical and blood group studies of sheep twin chimaeras

1970 ◽  
Vol 175 (1039) ◽  
pp. 183-200 ◽  
Keyword(s):  
Blood Cell ◽  
Blood Group ◽  
Sex Chromosomes ◽  
Cell Types ◽  
In Utero ◽  
Red Cells ◽  
Cell Populations ◽  
Red Cell ◽  
X Protein ◽  
Blood Grouping

Karyotyping and blood grouping methods were used to identify sheep twin chimaeras. Evidence that an exchange of blood cell precursors (the origin of chimaerism) had taken place in utero was obtained by examining lymphocytes in culture and finding the chromosomes of both sexes in one individual, or by finding admixture of red cell antigens, haemoglobin or ‘X ’ protein. Where chimaerism of sex chromosomes was found the pairs had identical red cell types, but two separate populations of red cells were not always identifiable. The four females in the pairs studied were freemartins. No correlation was found between the relative proportions of the two red cell populations and those of the two white cell populations. In one pair of chimaeric ewes, breeding tests showed that the major red cell populations in each case were the true genetic type. In the freemartins no correlation was found between the degree of masculinity and the numbers of male lymphocytes. A possible correlation of masculinity with red cell proportions is discussed.

scholarly journals Effect of oxalate and malonate on red cell metabolism

Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1389-1393
Author(s):  
E Beutler ◽  
L Forman ◽  
C West
Keyword(s):  
Pyruvate Kinase ◽  
Cell Metabolism ◽  
Inhibitory Effect ◽  
Red Cells ◽  
Red Cell ◽  
Acid Analogue ◽  
2,3 Dpg

The addition of oxalate to blood stored in Citrate-phosphate-dextrose (CPD) produces a marked improvement in 2,3-diphosphoglycerate (2,3-DPG) preservation; an increase in 2,3-DPG levels can also be documented in short-term incubation studies. Oxalate is a potent in vitro inhibitor of red cell lactate dehydrogenase, monophosphoglycerate mutase, and pyruvate kinase (PK). In the presence of fructose 1,6-diphosphate the latter inhibitory effect is competitive with phospho(enol)pyruvate (PEP). Determination of the levels of intermediate compounds in red cells incubated with oxalate suggest the presence of inhibition at the PK step, indicating that this is the site of oxalate action. Apparent inhibition at the glyceraldehyde phosphate dehydrogenase step is apparently due to an increase in the NADH/NAD ratio. Oxalate had no effect on the in vivo viability of rabbit red cells stored in CPD preservatives for 21 days. Greater understanding of the toxicity of oxalate is required before it can be considered suitable as a component of preservative media, but appreciation of the mechanism by which it affects 2,3-DPG levels may be important in design of other blood additives. Malonate, the 3-carbon dicarboxylic acid analogue of oxalate late did not inhibit pyruvate kinase nor affect 2,3-DPG levels.

scholarly journals The relationship between in vivo generated hemoglobin skeletal protein complex and increased red cell membrane rigidity

Blood ◽  
1988 ◽  
Vol 71 (5) ◽  
pp. 1427-1431 ◽  
Author(s):  
N Fortier ◽  
LM Snyder ◽  
F Garver ◽  
C Kiefer ◽  
J McKenney ◽  
...  
Keyword(s):  
Protein Complex ◽  
Sodium Dodecyl ◽  
Red Cells ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Cellular Dehydration ◽  
Thalassemia Minor ◽  
Membrane Rigidity

Abstract In vitro induced oxidative damage to normal human RBCs has previously been shown to result in increased membrane rigidity as a consequence of the generation of a protein complex between hemoglobin and spectrin. In order to determine if in vivo generated hemoglobin-spectrin complexes may play a role in increased membrane rigidity of certain pathologic red cells, we measured both these parameters in membranes prepared from hereditary xerocytosis (Hx), sickle cell disease (Sc), and red cells from thalassemia minor (beta thal). Membranes were prepared from density-fractionated red cells, and membrane deformability was measured using an ektacytometer. Hemoglobin-spectrin complex was determined by sodium dodecyl sulfate (SDS)-polyacrylamide gel analysis, as well as by Western blot analysis using a monoclonal antibody against the beta- subunit of hemoglobin. For these three types of pathologic red cells, progressive cellular dehydration was associated with increased membrane rigidity and increased content of hemoglobin-spectrin complex. Moreover, the increase in membrane rigidity appeared to be directly related to the quantity of hemoglobin-spectrin complex associated with the membrane. Our findings imply that hemoglobin-spectrin complex is generated in vivo, and this in turn results in increased membrane rigidity of certain pathologic red cells. The data further suggest that oxidative crosslinking may play an important role in the pathophysiology of certain red cell disorders.

scholarly journals The Role of Red Cell Energy Metabolism in the Generation of Irreversibly Sickled Cells In Vitro

Blood ◽  
1973 ◽  
Vol 42 (6) ◽  
pp. 835-842 ◽  
Author(s):  
Michael Jensen ◽  
Stephen B. Shohet ◽  
David G. Nathan
Keyword(s):  
Energy Metabolism ◽  
Calcium Metabolism ◽  
Red Cells ◽  
Red Cell ◽  
Hemoglobin S ◽  
Cell Energy ◽  
Incubation Buffer ◽  
Membrane Defect

Abstract An acquired membrane defect is believed to be responsible for the maintenance of the sickled shape in oxygenated irreversibly sickled cells (ISC), because the hemoglobin S in these cells is not in the aggregated, "sickled" state. In the present study, it is demonstrated that the acquisition of the membrane defect in vitro depends on cellular metabolism. Only if cellular ATP is almost completely depleted while the cells are sickled, do they become unable to resume the biconcave disk shape upon reoxygenation. If calcium is omitted from the incubation buffer, ISCs are not generated despite metabolic depletion. This suggests an action of ATP mediated through calcium metabolism similar to that which prevents membrane stiffening in normal red cells. No ISCs were produced by repeated sickling and unsickling. Thus, a membrane alteration occurring as a consequence of metabolic depletion seems to be a more important factor in the generation of ISC than sickling-unsickling induced fragmentation.

Sign in / Sign up

Export Citation Format

Share Document