The Effects of Thromboxane Antagonism on the Transit Time of Platelets Through the Spleen

Peters, A. M.; Lane, I. F.; Sinclair, M; Irwin, J. T. C.; McCollum, Charles

doi:10.1055/s-0038-1657881

Cited by 5 publications

(1 citation statement)

References 11 publications

(15 reference statements)

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“…The results was that the calculated rate of flow of platelets to the spleen was greater to maintain the same splenic content ( Table 4). The long splenic transit time and small flow rate constant for functional platelets (Table 4) resulted in platelet accumulation out of proportion to the splenic plasma volume (Peters et al 1985a;Kotz6 et al 1986). The long transit time of the functional platelets in the spleen could possibly be the result of the physical structure of the spleen, which slowed the platelets down in its pulp (Aster 1966;Peters et al 1983).…”

Section: Referencesmentioning

confidence: 99%

Blood platelet kinetics in normal subjects modelled by compartmental analysis

Sweetlove

Roodt

et al. 1992

Eur J Nucl Med

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The purpose of this study was to describe the function of platelets throughout their life span by expressing their in vivo distribution and kinetic behaviour in mathematical terms by using multicompartmental analysis. The distribution of indium-111 labelled platelets in five normal subjects was imaged and quantified with a scintillation camera image processing system. Serial blood samples were also obtained. The data were modelled using the SAAM (Simulation Analysis and Modelling) compartmental computer program. Five models were entertained to evaluate the role of platelets that were either functional or injured during collection and their interaction with the liver, spleen and vascular endothelium. Models were evaluated by comparing F values calculated from the least squares estimate obtained from each model. The Dornhorst function was used to describe the sequestration of platelets in the compartmental model. Results indicated that the data could not be satisfactorily simulated when compartments were included that simulated only functional and sequestered platelets (model 1). It was necessary to include compartments that simulated the kinetics of collection-injured platelets in the liver (model 2) and spleen (model 3). The model that simulated the interaction with the vascular endothelium (model 5) showed a visual but not significant improvement in the fitting of the observed data compared to model 3. The mean organ uptake and range indicated in parentheses were calculated at equilibrium. There were 20% (15%-27%) of the injected platelets in the spleen, 10% (8%-11%) in the liver and 70% (64%-75%) in the circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Referencesmentioning

confidence: 99%

Blood platelet kinetics in normal subjects modelled by compartmental analysis

Sweetlove

Roodt

et al. 1992

Eur J Nucl Med

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Thirty years of anti-mediator treatment in sepsis and septic shock - what have we learned?

Neugebauer

Rixen

Raum

et al. 1998

Langenbeck's Archives of Surgery

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Sepsis, the systemic response (specific and non-specific) of the body to an infection, is an increasing clinical problem. During the last 30 years, nearly 50 clinical trials involving more than 10,000 patients have failed to demonstrate improvement of patients' outcome with different "anti-mediator" strategies. The wrong conceptional approaches to interact with the complex mediator network and flaws in study design and conduct are the main reasons for this disappointing situation. We learned, however, that the systemic host response is more than persistent uncontrolled inflammation; it is also a stimulation of the counter regulatory network. Although it is important to analyse the complex picture, we have now reached a point where more sophisticated strategies for describing complexity and novel attempts for synthesis are needed. Along this line, improved study designs (decrease of "signal-to-noise ratio") are mandatory. In addition, secondary preventive strategies are emphasised.

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Splenic blood flow and intrasplenic platelet kinetics in relation to spleen volume

Wadenvik¹,

Denfors²,

Kutti³

1987

Br J Haematol

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Summary The relationship between the splenic blood flow and the intrasplenic platelet kinetics on the one hand, i.e. the two factors which govern the size of the exchangeable splenic platelet pool, and the spleen size on the other were assessed in 21 patients afflicted with haematologic disorders and variable splenomegaly. The splenic blood flow and intrasplenic platelet kinetics were measured using 111In‐labelled platelets and compartmental analysis of their equilibration between circulating blood and splenic pool; the spleen size was determined by scintigraphy using 99mTc‐labelled stannous colloid. Significant correlations were recorded between the spleen size and the splenic platelet pool size (r= 0.76; P<0.001) and between the spleen size and the splenic blood flow (r= 0.56; P<0.01). Splenic perfusion decreased significantly with increasing spleen size, but there was no relationship between the spleen size and the intrasplenic platelet transit time. However, an association was present between splenic perfusion and intrasplenic platelet transit time (r=—0.44; P<0.05). It is concluded that the splenic blood flow is the major determinant of the size of the exchangeable splenic platelet pool in splenomegalic states, and that the determination of spleen size using 99mTc‐scintigraphy gives a rough estimation of the pool size. Splenic perfusion appears to be one of the factors which determine the intrasplenic platelet transit time.

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The Effects of Thromboxane Antagonism on the Transit Time of Platelets Through the Spleen

Cited by 5 publications

References 11 publications

Blood platelet kinetics in normal subjects modelled by compartmental analysis

Blood platelet kinetics in normal subjects modelled by compartmental analysis

Thirty years of anti-mediator treatment in sepsis and septic shock - what have we learned?

Splenic blood flow and intrasplenic platelet kinetics in relation to spleen volume

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