scholarly journals THE RELATION OF THE RETICULO-ENDOTHELIAL SYSTEM TO THE BLOOD PLATELET COUNT

1926 ◽  
Vol 44 (1) ◽  
pp. 75-83 ◽  
Author(s):  
Harry Koster

1. So called blockade of the reticulo-endothelial system results in a marked increase in the platelet count. 2. The count rapidly becomes very high, shows a sharp partial recoil and then a gradual diminution even though the blockade be continued. 3. The mechanism regulating the number of platelets is a complicated one. 4. Apparently phagocytosis by cells of the reticulo-endothelial system is not the only means by which blood platelets are destroyed.

2016 ◽  
Vol 3 (2) ◽  
pp. 81
Author(s):  
Hieronymus Rayi Prasetya ◽  
Maria Irena Dentri ◽  
Sistiyono Sistiyono

Background: Platelets play a role in hemostasis which is the body's mechanisms to prevent and stop the bleeding. Platelets participate in the effort to close the wound, so that the body does not experience a loss of blood and protected from foreign cells. Examination of the platelet count is very important in the diagnosis of diseases, one of which is the diagnosis of dengue hemorrhagic fever (DHF). Examination of blood counts, especially platelets in clinical laboratories causes blood samples in use are not always the venous blood but could use capillary blood. Capillary blood samples are used primarily in pediatric patients, because the venous blood sampling is difficult, patient loads, and also shorten the time when taking blood. The purpose of this study was to determine whether there is a difference in counting the number of platelets using samples of blood veins and capillaries. Methods: Quantitative research with observational approach using a cross sectional study design in the 30 samples of student D3 Health Analyst STIKes To Nation Yogyakarta. Statistical methods in use are independent T test. Results: The research subjects were 30 samples of student D3 Health Analyst STIKes To Nation Yogyakarta. The results of the examination of venous blood platelet count and blood capillaries have different average values ​​are 247 530 cells / ml of blood, for blood platelets veins and 184 270 cells / ml of blood for capillary blood platelets. Spearman correlation analysis Obtained results of the examination of venous blood platelet count and blood capillaries normal distribution (p> 0.05). 0.129 venous blood platelet counts, while the number of blood platelets kapilernya 0.089. Conclusion: There is a significant difference from the results of counting the number of blood platelets using veins and capillaries, where the use of capillary blood samples showed that lower platelet counts.


1979 ◽  
Author(s):  
D.G. Meuleman ◽  
G.M.T. Vogel ◽  
van A.M.L. Delft

Blood platelets play probably an important role in the occurrence of stroke. We determined the survival of radiolabelled blood platelets, the blood platelet count and blood pressure in male stroke prone, spontaneously hypertensive rats during ageing. Our investigations revealed that 1) blood pressure starts to rise at an early age (8 weeks) reaching a steady state (approx. 250 mmHg) at 15-20 weeks of age, 3) blood platelet count is steadily decreasing from 9 weeks of age on, reaching a steady state (approx. 50% of the original platelet count) at 20 weeks of age, 3) blood platelet survival is gradually shortening from 12 weeks of age on, reaching a steady shortened half-life of 18 hours (normal value approx. 42 hours). It is concluded that the rise in blood pressure induces at first instance a moderately increased platelet consumption, which is not compensated by an increased platelet production and which is not detectable by platelet survival measurement. In a later phase, when the blood pressure is in a steady state, platelet consumption is further increased, leading to significantly shortened platelet survivals. This process is then compensated by increased platelet production leading to a steady state thrombocytopenia.


1978 ◽  
Vol 39 (02) ◽  
pp. 346-359 ◽  
Author(s):  
P D Winocour ◽  
M R Turner ◽  
T G Taylor ◽  
K A Munday

SummaryA major limitation to single-cell protein (SCP) as a human food is its high nucleic acid content, the purine moiety of which is metabolised to uric acid. Rats given a Fusarium mould as a source of SCP in diets containing oxonate, a uricase inhibitor, showed elevated plasma and kidney uric acid concentrations after 21 d, which were related to the level of dietary mould. ADP-induced and thrombin-induced platelet aggregation was greater in the hyperuricaemic rats than in controls and a progressive increase in aggregation with increasing levels of dietary mould was observed. Furthermore a time-lag, exceeding the life-span of rat platelets, was observed between the development of hyperuricaemia and the increase in aggregation. A similar time-lag was observed between the lowering of the hyperuricaemia and the reduction of platelet aggregation when oxonate was removed from the diet.If human platelets react to uric acid in the same manner as rat platelets this might explain the link that has been suggested between hyperuricaemia and ischaemic heart disease. In that event diets high in nucleic acids might be contra-indicated in people at risk from ischaemic heart disease.In rats given a low protein diet (50 g casein/kg) for 21 d ADP-induced and thrombin-induced platelet aggregation and whole blood platelet count were reduced compared with control animals receiving 200 g casein/kg diet but not in rats given 90 or 130 g casein/kg diet. A study of the time course on this effect indicated that the reduction both in aggregation tendency and in whole blood platelet count occurred after 4 d of feeding the low protein diet. These values were further reduced with time.


Blood ◽  
1952 ◽  
Vol 7 (9) ◽  
pp. 948-949 ◽  
Author(s):  
KENNETH OTTIS ◽  
OSCAR E. TAUBER

Abstract Healthy, adult male and female golden hamsters, 3 months of age, showed blood platelet count means of 688,000 ± 141,000 per cu. mm. and 742,000 ± 120,000 per cu. mm., respectively, when direct counts were made with siliconized pipets and with Rees and Ecker fluid as a diluent.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2892-2892
Author(s):  
Larry J. Dumont ◽  
L. Lassahn ◽  
Peter A. Tomasulo ◽  
Dennis Harpool ◽  
S. Pinkard ◽  
...  

Abstract BACKGROUND: Apheresis platelet collection from healthy normal blood donors can reduce the donor peripheral blood platelet concentration by 50% or more. The kinetics of peripheral blood platelet count (PLT) recovery in the apheresis donors over the first 24 hours has not been described. The objective of this study was to determine the recovery kinetics of the donor peripheral blood platelet count following apheresis platelet donation. METHODS: Healthy apheresis platelet donors were enrolled following informed consent. The apheresis platelet collection was performed using the Gambro Trima system (Gambro BCT, Lakewood, CO) following local SOP and manufacturer’s directions for use. The minimum predicted post-count was configured in the Trima to no less than 78K plt/μL. PLT was determined pre-procedure (Pre), immediately post procedure (Post), 4–11 h (FU1) and 11–41 h (FU2) post-donation using standard methods. The PLT recovery was evaluated as the increase in PLT following the donation (Delta). The effects of study site, time of sample, and the fraction of platelets collected (Fpc) at donation on Delta were evaluated using a random effects generalized linear regression model. A full regression model of Delta as a function of study site, follow-up period and Fpc with all main and interaction effects was used to test hypotheses. RESULTS: 548 subjects were entered into the study at 3 study sites; Pre-PLT 276±59 × 103 plt/μL, Post-PLT 205±47 × 103 plt/μL, Fpc 25±10%. No adverse events were reported by any subjects. Recovery of platelet count following apheresis platelet donation is variable between subjects; and the independent variables of study site, follow-period and Fpc accounted for 25% of the total variation in Delta. PLT increased 12.4±0.9 × 103 plt/μL by the time of follow-up sampling (p=0.01), although there was no difference between PLT at FU1 (214±49 × 103 plt/μL) and FU2 (212±47 × 103 plt/μL; p=0.15). None of the donors reached their pre-donation platelet count during the follow-up period. There was no difference in Delta between centers (p=0.23). Fpc had a significant affect on Delta (p<0.0001); with estimated Delta of 5.2±0.9 × 103 plt/μL at Fpc=15% and 16.0±.8 × 103 plt/μL at Fpc=30%. CONCLUSION: Platelet recovery following apheresis platelet donation was observed to be dependent on the fraction of platelets donated. Surprisingly, the recovery observed within the first 11 h was equivalent to that observed between 11–42 h, averaging 17.5% of the drop observed during apheresis. Recovery was not complete when observed for up to 41 h following donation in this study. Additional investigation of PLT recovery following apheresis donation is indicated to describe and differentiate the potential roles of de novo production, early pro-platelet release and platelet release from peripheral pools over the early post-donation period.


2010 ◽  
Vol 31 (4) ◽  
pp. 258-262 ◽  
Author(s):  
M Eskola ◽  
S Juutistenaho ◽  
K Aranko ◽  
S Sainio ◽  
R Kekomäki

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