scholarly journals INTRAVASCULAR HEMAGGLUTINATION

Blood ◽  
1950 ◽  
Vol 5 (12) ◽  
pp. 1114-1124 ◽  
Author(s):  
RICHARD DAY ◽  
ELISE PERRY
Keyword(s):  
Oxygen Consumption ◽  
Hemolytic Anemia ◽  
Sedimentation Rate ◽  
The Other ◽  
Red Cell ◽  
Tissue Oxygen ◽  
Total Oxygen ◽  
Cell Agglutination ◽  
Additional Support

Abstract Severe degrees of intravascular red cell agglutination have been observed during life in rats injected with anti-rat red cell serum and in a patient of 11 months with chronic acquired hemolytic anemia. There was no significant fall in the tissue oxygen tension or in the total oxygen consumption of the rats. Neither the rats nor the infant developed kernicterus. In a baby dying with kernicterus no true hemagglutination was observed, although there was slight sludging such as is seen in many illnesses. Additional support for the belief that the red cells in this case were not clumped lies in the fact that in vitro clumping was not observed; furthermore, the sedimentation rate was only 1 mm. in one hour. The blood of the injected rats and of the other infant who did not develop kernicterus sedimented extremely rapidly and displayed spontaneous agglutination in vitro. These observations indicate that intravascular agglutination has little if any bearing on the development of kernicterus in erythroblastosis fetalis.

scholarly journals Oxygen Consumption of the Isolated Heart of Octopus: Effects of Power Output and Hypoxia

1987 ◽  
Vol 131 (1) ◽  
pp. 137-157
Author(s):  
D. F. HOULIHAN ◽  
C. AGNISOLA ◽  
N. M. HAMILTON ◽  
I. TRARA GENOINO
Keyword(s):  
Oxygen Consumption ◽  
Output Power ◽  
Power Output ◽  
Isolated Heart ◽  
Back Pressure ◽  
Octopus Vulgaris ◽  
Total Oxygen ◽  
Coronary Veins ◽  
Output Flow

A technique is described which allowed the measurement of the oxygen consumption of the isolated heart of Octopus vulgaris. Contraction of the heart resulted in an aortic output and a flow through the heart muscle into coronary veins (the coronary output). The flow and oxygen content of the aortic output and the coronary output were measured with variable input pressures and constant output back pressure (volume loaded), variable output back pressure and constant aortic output (pressure loaded), and during hypoxia. Volume loading of the heart resulted in an increase in aortic output, power output and total oxygen consumption. Pressure loading increased power output and total oxygen consumption of the heart. Exposure to hypoxia decreased the aortic output, power output and total cardiac oxygen consumption. In the response of the heart to reduced work, brought about either by a reduced input pressure or by hypoxic perfusate, the power output was linearly related to the total oxygen consumption of the heart. The oxygen extracted from the coronary output accounted for 80–100% of the total oxygen consumption of the heart. Coronary output amounted to 30% of the total cardiac output at maximum power output. In volume-loaded hearts the volume of the coronary output increased as aortic output increased; in pressure-loaded hearts coronary output increased as power output increased, but aortic output remained constant. In hypoxia, the coronary output increased as the aortic output fell. At a perfusate Po2 of around 50 Torr (1 Torr = 133 Pa), the aortic output ceased although the heart continued to beat and the coronary output continued, accounting for all of the oxygen consumption of the heart. The coronary output flow in vitro therefore has the capacity to be varied independently of the aortic output flow to maintain the oxygen supply to the perfused cardiac muscle.

scholarly journals The fuel of the spleen. Studies using a new method for perfusing the rat spleen with whole blood

1989 ◽  
Vol 263 (2) ◽  
pp. 325-332 ◽  
Author(s):  
M A Mindham ◽  
P A Mayes
Keyword(s):  
Oxygen Consumption ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Whole Blood ◽  
Glucose Oxidation ◽  
The Other ◽  
Cell Populations ◽  
Total Oxygen ◽  
Total Glucose ◽  
Oxidation Of Glucose

1. An improved rat spleen perfusion is described incorporating a method of defibrination which avoids the use of heparin and enables the spleen to be perfused with rat blood for several hours at a haematocrit of 40% and for 12 h or more at a haematocrit of 20%. 2. Glucose oxidation accounted for 11.6% of the total oxygen consumption but this represented only 8% of total glucose uptake, which was largely converted to lactate and released into the perfusate. However, significant amounts of lactate were oxidized. These results can be explained by the presence of at least two cell populations, one emphasizing the anaerobic oxidation of glucose and the other aerobic metabolism, particularly of lactate. 3. Non-esterified fatty acid and 3-hydroxybutyrate, when available at physiological concentrations, were shown to be major oxidative fuels of the spleen. 4. Chylomicron triacylglycerol was hydrolysed readily and taken up, but not oxidized extensively.

scholarly journals Artificially Induced Thyroid Suppression in Sickle Cell Disease

Blood ◽  
1972 ◽  
Vol 40 (6) ◽  
pp. 905-913
Author(s):  
Charles W. Seward ◽  
John W. Eaton ◽  
Hugh Chaplin
Keyword(s):  
Oxygen Consumption ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Clinical Status ◽  
Cell Mass ◽  
Musculoskeletal Symptoms ◽  
Red Cell ◽  
Cell Disease ◽  
Tissue Oxygen ◽  
Tissue Oxygen Consumption

Abstract Depression of thyroid function in patients with hemoglobin SS disease might be expected to: (1) reduce tissue oxygen consumption, (2) decrease erythrocyte 2, 3-diphosphoglycerate, (3) decrease p50, (4) increase the average level of erythrocyte oxygenation, and (5) increase in vivo red cell survival with associated improvement in anemia and possibly in musculoskeletal symptoms. Accordingly, 150-200 mg of 6-n-propylthiouracil were administered three times a day for 143 days to a 21-yr-old male with hemoglobin SS disease. Thyrosuppression was indicated by typical symptoms and appropriate changes in physical and biochemical parameters. Detailed hematologic follow-up, including multiple measurements of red cell mass, 51Cr erythrocyte survival, red cell 2,3-diphosphoglycerate, and p50, showed no change. Furthermore, musculoskeletal symptoms continued in the pattern characteristic of the euthyroid state. A possible explanation for the lack of any change in clinical status may be that decreased cardiac output, with attendant prolonged circulation time and increased tissue oxygen demand per red cell per unit time, offset the absolute decrease in tissue oxygen consumption. The study provided an opportunity to make detailed clinical observations of sickle cell disease in association with thyroid suppression. The results suggest that thyrosuppression within the limits of symptomatic and physiologic tolerance has no therapeutic application in the clinical management of hemoglobin SS disease.

scholarly journals STUDIES ON THE INTERACTION BETWEEN PHAGOCYTES AND TUBERCLE BACILLI

1956 ◽  
Vol 104 (1) ◽  
pp. 137-150 ◽  
Author(s):  
Hartmann Stähelin ◽  
Manfred L. Karnovsky ◽  
Emanuel Suter
Keyword(s):  
Carbon Dioxide ◽  
Bacillus Subtilis ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
Guinea Pigs ◽  
Significant Degree ◽  
The Other ◽  
Polymorphonuclear Leucocytes ◽  
Mycobacterium Phlei

Tubercle bacilli labelled with C14 were prepared by growth on radioactive substrates such as glycerol, CO2, and acetate. These organisms were exposed in vitro to leucocytes (mostly polymorphonuclear leucocytes) from peritoneal exudates of guinea pigs. The respiration of the leucocytes and of the bacilli, alone and together, was followed by determining oxygen uptake and C14O2 production. When heat-killed labelled tubercle bacilli were exposed to leucocytes there was little or no degradation of bacillary material to C14O2 by leucocytic enzymes. On the other hand, conversion of components of sonically disrupted bacilli to C14O2 by leucocytes was significant. It was possible to determine the oxygen uptake and C14O2 production of phagocytized living tubercle bacilli, and it was found that after phagocytosis the bacilli maintained their rates of oxygen consumption and C14O2 production. This finding was in contrast to observations made with Mycobacterium phlei, a saprophytic acid-fast organism, and with Bacillus subtilis. In these cases oxygen consumption and C14O2 production declined after phagocytosis, and bacterial components were converted to carbon dioxide to a significant degree by leucocytic enzymes.

Cow red blood cells. I. Effect of purines, pyrimidines, and nucleosides in bovine red cell glycolysis

1979 ◽  
Vol 236 (5) ◽  
pp. C255-C261 ◽  
Author(s):  
M. J. Seider ◽  
H. D. Kim
Keyword(s):  
Pyruvate Kinase ◽  
Enzyme Activities ◽  
Blood Cells ◽  
Glycolytic Enzyme ◽  
Red Cells ◽  
The Other ◽  
Red Cell ◽  
Hexokinase Activity ◽  
Glycolytic Rate

Cow red cells, under in vitro incubation conditions, exhibit a comparatively low glycolytic rate of 0.56 +/- 0.05 micromol/(ml cells.h), with a ratio of lactate formed to glucose consumed of 1.58. It has been found that this low glycolytic rate can be stimulated 50--60% above the basal level in the presence of a variety of purine and pyrimidine compounds including adenosine, inosine, adenine, hypoxanthine, xanthine, and uracil. In contrast, calf red cells, which have a much higher glycolytic rate, display no discernible response to these agents. In attempts to elucidate the mechanism by which this stimulation takes place, both glucose transport and glycolytic enzyme activities were determined in the presence of these stimulators. Glucose influx in cow red cells, measured using the glucose analog 3-O-methyl-glucose, exhibits both a low Km of 117 microM and a Vmax of 0.38 micromol/(ml cells.min), and is unaltered in the presence of adenosine. On the other hand, hexokinase, which in normal hemolysates of cow red cells has an activity of 0.49 +/- 0.03 micromol/(g Hb.min). was found to be stimulated to 0.73 micromol/(g Hb.min) in the presence of adenine. Both pyruvate kinase and phosphofructokinase were unaffected by this compound. These data suggest that certain purines and pyrimidine compounds may exert their stimulatory effect on hexokinase activity, resulting in an augmentation of cow red cell glycolysis.

scholarly journals Globulin Coating of Neoplastic Lymphocytes in Chronic Lymphocytic Leukemia

Blood ◽  
1963 ◽  
Vol 22 (2) ◽  
pp. 139-151 ◽  
Author(s):  
JEROME I. BRODY ◽  
LAWRENCE H. BEIZER
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Hemolytic Anemia ◽  
Lymphocytic Leukemia ◽  
Normal Lymphocyte ◽  
Temperature Dependent ◽  
Cell Agglutination ◽  
Mixed Cell ◽  
Neoplastic Lymphocytes ◽  
Immunologic Reactions

Abstract 1. Employing the technic of specific mixed cell agglutination (SMCA), it has been demonstrated that leukemic lymphocytes, as well as red cells, may be coated with globulins which are reactive with antihuman (Coombs) serum. 2. Moreover, in vitro, these proteins may dissociate from neoplastic lymphocytes and reassociate on normal erythrocytes rendering them Coombs-positive. 3. The dissociation-reassociation phenomenon appears to be time- and temperature-dependent and may be augmented by complement or a related heat-labile serum or cell factor. 4. It is suggested, by analogy to instances in which the normal lymphocyte mediates certain immunologic reactions, that the neoplastic lymphocyte may participate actively in the acquired hemolytic anemia of chronic lymphocytic leukemia.

scholarly journals Correlations Between Quantitative Assay of Red Cell-bound C3, Serologic Reactions, and Hemolytic Anemia

Blood ◽  
1974 ◽  
Vol 44 (3) ◽  
pp. 359-373 ◽  
Author(s):  
Jörg Th. Fischer ◽  
Lawrence D. Petz ◽  
George Garratty ◽  
Neil R. Cooper
Keyword(s):  
Hemolytic Anemia ◽  
Red Cells ◽  
Simple Extension ◽  
Red Cell ◽  
Immunochemical Method ◽  
Antiglobulin Test ◽  
Degree Of Sensitization ◽  
Human Immune

Abstract A new immunochemical method was used to quantitate the number of C3 molecules bound to human red cells in vitro or in vivo and to assess the clinical significance of cell-bound C3 in immune hemolysis. In addition, results utilizing the immunochemical method were compared with those obtained using commonly performed semiquantitative serologic techniques such as the antiglobulin test and antiglobulin titration score. The antiglobulin test using anti-C3 antiglobulin serum became weakly positive with 60-115 molecules C3 per red cell, and was strongly positive with 1000 molecules C3 per red cell. Antiglobulin titration scores correlate well with immunochemical assessment of the number of C3 molecules per red cell. Therefore, a simple extension of the routine antiglobulin test affords clinically useful data concerning the relative degree of sensitization of red cells by C3. Two of fourteen patients with fewer than 1100 molecules C3 per red cell had hemolytic anemia, whereas 8 of 11 patients with greater than 1100 molecules C3 per red cell had overt hemolysis. The presence or absence of hemolysis was not explained by variations in the amount of IgG on these patients’ RBC. It thus appears that the amount of C3 per red cell is an important determinant of hemolysis in human immune hemolytic anemias.

scholarly journals Congenital Hemolytic Disease Associated with Red Cell Inclusion Bodies, Abnormal Pigment Metabolism and an Electrophoretic Hemoglobin Abnormality

Blood ◽  
1960 ◽  
Vol 16 (3) ◽  
pp. 1239-1252 ◽  
Author(s):  
J. L. SCOTT ◽  
A. HAUT ◽  
G. E. CARTWRIGHT ◽  
M. M. WINTROBE
Keyword(s):  
Hemolytic Anemia ◽  
Inclusion Bodies ◽  
Red Cell ◽  
Hemolytic Disease ◽  
Genetic Transmission ◽  
Fourth Case ◽  
In Vitro Incubation ◽  
Partial Correction ◽  
Congenital Hemolytic Anemia

Abstract 1. A fourth case of the syndrome of congenital hemolytic anemia with abnormal pigment metabolism and red cell inclusion bodies following splenectomy is described. 2. In this case an abnormality was found on paper and starch electrophoresis of the red cell hemolysate at pH 8.6. A similar abnormality has not been reported previously. 3. An increased rate of erythrocyte autohemolysis was found during in vitro incubation, Partial correction of this defect occurred in the presence of glucose or purine ribosides. 4. Genetic transmission of the defect could not be demonstrated.

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