Optimal volume of anticoagulant citrate dextrose solution in the preparation of technetium Tc 99m-labeled red blood cells

1994 ◽  
Vol 51 (21) ◽  
pp. 2699-2701
Author(s):  
Joseph C. Hung ◽  
Mark F. Wilson
Author(s):  
Dr. Sirat Kaur

Red blood cells are still the most widely transfused blood component worldwide and their story is intimately entwined with the history of transfusion medicine and the changes in the collection and storage of blood.1,2 At present, the most widely used protocol for the storage of red blood cells (for up to 42 days) is the collection of blood into anticoagulant solutions (typically citrate-dextrose-phosphate); red cell concentrates are prepared by the removal of plasma and, in some cases, also leukoreduction. The product is stored at 4 ± 2° C in a slightly hypertonic additive solution, generally SAGM (sodium, adenine, glucose, mannitol, 376 mOsm/L).1 The British obstetrician, Braxton Hicks in 1868, experimented with a solution of phosphate of soda, but this also proved toxic. Richard Lewinsohn, in 1915, of the Mount Sinai Hospital in New York is credited with introducing sodium citrate into clinical practice as an anticoagulant.3In fact, a 1% solution of sodium citrate was already widely used in laboratories as an anticoagulant. This high concentration was toxic to humans but, as Lewinsohn himself recalled, `Nobody had ever followed the simple thought of carrying out experiments to ascertain whether a much smaller dose might not be sufficient' for use as an anticoagulant.


Author(s):  
Kosuke Ueda ◽  
Hiroto Washida ◽  
Nakazo Watari

IntroductionHemoglobin crystals in the red blood cells were electronmicroscopically reported by Fawcett in the cat myocardium. In the human, Lessin revealed crystal-containing cells in the periphral blood of hemoglobin C disease patients. We found the hemoglobin crystals and its agglutination in the erythrocytes in the renal cortex of the human renal lithiasis, and these patients had no hematological abnormalities or other diseases out of the renal lithiasis. Hemoglobin crystals in the human erythrocytes were confirmed to be the first case in the kidney.Material and MethodsTen cases of the human renal biopsies were performed on the operations of the seven pyelolithotomies and three ureterolithotomies. The each specimens were primarily fixed in cacodylate buffered 3. 0% glutaraldehyde and post fixed in osmic acid, dehydrated in graded concentrations of ethanol, and then embedded in Epon 812. Ultrathin sections, cut on LKB microtome, were doubly stained with uranyl acetate and lead citrate.


Author(s):  
John A. Trotter

Hemoglobin is the specific protein of red blood cells. Those cells in which hemoglobin synthesis is initiated are the earliest cells that can presently be considered to be committed to erythropoiesis. In order to identify such early cells electron microscopically, we have made use of the peroxidatic activity of hemoglobin by reacting the marrow of erythropoietically stimulated guinea pigs with diaminobenzidine (DAB). The reaction product appeared as a diffuse and amorphous electron opacity throughout the cytoplasm of reactive cells. The detection of small density increases of such a diffuse nature required an analytical method more sensitive and reliable than the visual examination of micrographs. A procedure was therefore devised for the evaluation of micrographs (negatives) with a densitometer (Weston Photographic Analyzer).


Author(s):  
Victor Tsutsumi ◽  
Adolfo Martinez-Palomo ◽  
Kyuichi Tanikawa

The protozoan parasite Entamoeba histolytica is the causative agent of amebiasis in man. The trophozoite or motile form is a highly dynamic and pleomorphic cell with a great capacity to destroy tissues. Moreover, the parasite has the singular ability to phagocytize a variety of different live or death cells. Phagocytosis of red blood cells by E. histolytica trophozoites is a complex phenomenon related with amebic pathogenicity and nutrition.


Author(s):  
D.J.P. Ferguson ◽  
A.R. Berendt ◽  
J. Tansey ◽  
K. Marsh ◽  
C.I. Newbold

In human malaria, the most serious clinical manifestation is cerebral malaria (CM) due to infection with Plasmodium falciparum. The pathology of CM is thought to relate to the fact that red blood cells containing mature forms of the parasite (PRBC) cytoadhere or sequester to post capillary venules of various tissues including the brain. This in vivo phenomenon has been studied in vitro by examining the cytoadherence of PRBCs to various cell types and purified proteins. To date, three Ijiost receptor molecules have been identified; CD36, ICAM-1 and thrombospondin. The specific changes in the PRBC membrane which mediate cytoadherence are less well understood, but they include the sub-membranous deposition of electron-dense material resulting in surface deformations called knobs. Knobs were thought to be essential for cytoadherence, lput recent work has shown that certain knob-negative (K-) lines can cytoadhere. In the present study, we have used electron microscopy to re-examine the interactions between K+ PRBCs and both C32 amelanotic melanoma cells and human umbilical vein endothelial cells (HUVEC).We confirm previous data demonstrating that C32 cells possess numerous microvilli which adhere to the PRBC, mainly via the knobs (Fig. 1). In contrast, the HUVEC were relatively smooth and the PRBCs appeared partially flattened onto the cell surface (Fig. 2). Furthermore, many of the PRBCs exhibited an invagination of the limiting membrane in the attachment zone, often containing a cytoplasmic process from the endothelial cell (Fig. 2).


2001 ◽  
Vol 120 (5) ◽  
pp. A356-A357
Author(s):  
M FURUKAWA ◽  
Y MAGAMI ◽  
D NAKAYAMA ◽  
F MORIYASU ◽  
J PARK ◽  
...  

1990 ◽  
Vol 63 (01) ◽  
pp. 112-121 ◽  
Author(s):  
David N Bell ◽  
Samira Spain ◽  
Harry L Goldsmith

SummaryThe effect of red blood cells, rbc, and shear rate on the ADPinduced aggregation of platelets in whole blood, WB, flowing through polyethylene tubing was studied using a previously described technique (1). Effluent WB was collected into 0.5% glutaraldehyde and the red blood cells removed by centrifugation through Percoll. At 23°C the rate of single platelet aggregtion was upt to 9× greater in WB than previously found in platelet-rich plasma (2) at mean tube shear rates Ḡ = 41.9,335, and 1,920 s−1, and at both 0.2 and 1.0 µM ADP. At 0.2 pM ADP, the rate of aggregation was greatest at Ḡ = 41.9 s−1 over the first 1.7 s mean transit time through the flow tube, t, but decreased steadily with time. At Ḡ ≥335 s−1 the rate of aggregation increased between t = 1.7 and 8.6 s; however, aggregate size decreased with increasing shear rate. At 1.0 µM ADP, the initial rate of single platelet aggregation was still highest at Ḡ = 41.9 s1 where large aggregates up to several millimeters in diameter containing rbc formed by t = 43 s. At this ADP concentration, aggregate size was still limited at Ḡ ≥335 s−1 but the rate of single platelet aggregation was markedly greater than at 0.2 pM ADP. By t = 43 s, no single platelets remained and rbc were not incorporated into aggregates. Although aggregate size increased slowly, large aggregates eventually formed. White blood cells were not significantly incorporated into aggregates at any shear rate or ADP concentration. Since the present technique did not induce platelet thromboxane A2 formation or cause cell lysis, these experiments provide evidence for a purely mechanical effect of rbc in augmenting platelet aggregation in WB.


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