The Effect of Partial Splenectomy on Platelet Production in Mice

1981 ◽  
Vol 46 (03) ◽  
pp. 602-603 ◽  
Author(s):  
H Bessler ◽  
I Notti ◽  
M Djaldetti

SummaryThe effect of total and partial splenectomy on the number and production of circulating platelets was studied in mice. Five days after total and partial splenectomy the number of the peripheral blood platelets increased by 87% and 60%, respectively and the incorporation of 75selenium methionine (75Se-Met) into platelets was enhanced indicating that the thrombocytosis was due to increased platelet production. The results obtained by the two operative procedures were compared.Since previous work from our laboratory has shown that a factor produced by splenic lymphocytes affects the platelet number in mice, it is suggested that the differences in the number of circulating platelets observed in animals after total and partial splenectomy may reflect a difference in the number of spleen lymphocytes removed.

2020 ◽  
Vol 21 (20) ◽  
pp. 7591
Author(s):  
Emma C. Josefsson ◽  
William Vainchenker ◽  
Chloe James

Blood platelets have important roles in haemostasis, where they quickly stop bleeding in response to vascular damage. They have also recognised functions in thrombosis, immunity, antimicrobal defense, cancer growth and metastasis, tumour angiogenesis, lymphangiogenesis, inflammatory diseases, wound healing, liver regeneration and neurodegeneration. Their brief life span in circulation is strictly controlled by intrinsic apoptosis, where the prosurvival Bcl-2 family protein, Bcl-xL, has a major role. Blood platelets are produced by large polyploid precursor cells, megakaryocytes, residing mainly in the bone marrow. Together with Mcl-1, Bcl-xL regulates megakaryocyte survival. This review describes megakaryocyte maturation and survival, platelet production, platelet life span and diseases of abnormal platelet number with a focus on the role of Bcl-xL during these processes.


Blood ◽  
1978 ◽  
Vol 51 (4) ◽  
pp. 601-610 ◽  
Author(s):  
CA Pugsley ◽  
IJ Forbes ◽  
AA Morley

Abstract The immunology of chronic hypoplastic marrow failure (CHMF, aplastic anemia) was studied in an experimental murine model of the disease induced by busulfan. B lymphocytes of peripheral blood, spleen, and bone marrow were reduced to 30%–40% and T lymphocytes of thymus, spleen, marrow, and blood were decreased to 20%–70% of control values. IgG and IgM antibody titer to sheep red blood cells were reduced to one- third of control levels, and splenic IgG, but not IgM, plaque-forming cells were fewer on day 7 after antigen stimulation. The proliferative responses to phytohemagglutinin or concanavalin A were reduced in cultures of peripheral blood lymphocytes, splenic lymphocytes, and thymocytes, and cutaneous delayed-type hypersensitivity induced by dinitrofluorobenze was not detected in mice with CHMF. The results demonstrate disturbance of a variety of cellular and humoral functions and suggest that the disturbance was due to quantitative and possibly qualitative abnormalities of the cell types subserving these functions. The results suggest that residual cell injury, the lesion underlying experimental CHMF, is not confined to the myeloid stem cell but also involved cells of the lymphoid series.


1991 ◽  
Vol 32 (6) ◽  
pp. 335-341 ◽  
Author(s):  
Yoshinori Nio ◽  
Takahiro Shiraishi ◽  
Michihiko Tsubono ◽  
Hideki Morimoto ◽  
Chen-Chiu Tseng ◽  
...  

1977 ◽  
Vol 36 (6) ◽  
pp. 777-782 ◽  
Author(s):  
P D Jones ◽  
T E Sadler ◽  
J E Castro

Blood ◽  
1986 ◽  
Vol 67 (6) ◽  
pp. 1705-1709 ◽  
Author(s):  
LE Silberstein ◽  
GA Robertson ◽  
AC Harris ◽  
L Moreau ◽  
E Besa ◽  
...  

Abstract This study investigated the clonal nature of cold agglutinin disease in a series of nine patients, which included the benign or idiopathic form as well as cases with an underlying lymphoma. Surface marker phenotyping and karyotypic analysis were performed on peripheral blood lymphocytes. An increased proportion of B cells was found in four cases and in three of these patients a monoclonal B cell population was identified with a mu, kappa phenotype. In the same three cases, as well as an additional patient, an aberrant karyotype was demonstrated. The cytogenetic abnormality present in all four cases included trisomy 3; two patients also had a trisomy 12. One of these four patients had a well-differentiated lymphoma and underwent a splenectomy. Splenic lymphocytes were transformed with Epstein-Barr virus and cultured en masse. Eight clones were established producing the same cold agglutinin with identical specificity as that present in the patient's plasma. Five of these clones were studied cytogenetically, and all had the same abnormal karyotype (51,XX,+3,+9,+12,+13,+18) found in peripheral blood and splenic lymphocytes. Thus, in this case, the cold reactive autoantibody was produced by the chromosomally abnormal, neoplastic clone of lymphocytes. Our findings support the view that cold agglutinin disease represents a spectrum of clonal disorders.


1979 ◽  
Vol 16 (2) ◽  
pp. 229-242 ◽  
Author(s):  
C. M. Forsberg ◽  
V. E. O. Valli ◽  
P. W. Gentry ◽  
R. M. Donworth

Blood coagulation studies showed there was a pronounced thrombocytopenia and hypofibrinogenemia in Holstein calves infected with Trypanosoma congolense TREU 112. There was also ineffective thrombopoiesis characterized by an increased megakaryocytic mass, reduced uptake of 35S-methionine into peripheral blood platelets and a normal platelet lifespan. There was an increased uptake of isotopic label into fibrinogen and a shortened half life indicating a consumptive error with increased peripheral use of fibrinogen. No consistent abnormalities were found in ethanol gelation, partial thromboplastin time, clot retraction and lysis or plasminogen assay. Fibrin split products were rarely detected. These findings suggest that in the chronic form of bovine trypanosomiasis there is a partially compensated consumption coagulopathy.


1977 ◽  
Author(s):  
Z. Jerushalmy ◽  
M. Patya ◽  
O. Sperling

Human blood platelets were gtudied for the presence of the pathway of de novo synthesis of purine nucleotides. 8 x 108 cells were incubated for 2.5 h at 37°C in 2 ml of Eagle’s Minimal Essential Medium containing Earle’s Balanced Salt Solution, 15% fetal calf serum and 20 μCi sodium [14C] formate (59 mCi/mmole). Platelets were found to incorporate 14C into total purines at a slow but detectable rate of 50–70 pmoles/8 x 108 cells/2.5 h. This incorporation was inhibited by approximately 80% at 10 mM azaserine and by 60% at 0.1 mM adenine. Adenine is known to affect the rate of purine synthesis de novo through the activity of phosphoribosylpyrophosphate amidotransferase, the first committed enzyme of this pathway. The results suggest the presence of the complete pathway of de novo synthesis of purine nucleotides in normal human peripheral blood platelets.


1986 ◽  
Vol 8 (3) ◽  
pp. 345-355 ◽  
Author(s):  
James D. Tucker ◽  
Cheryl L. Strout ◽  
Mari L. Christensen ◽  
Anthony V. Carrano

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