Acquired platelet storage container leaks and contamination with environmental bacteria: A preventable cause of bacterial sepsis

Comparison between a new PVC platelet storage container (UPX80) and a polyolefin container

Transfusion Medicine ◽

10.1046/j.1365-3148.2000.00243.x ◽

2000 ◽

Vol 10 (2) ◽

pp. 131-139 ◽

Cited By ~ 16

Author(s):

Kostelijk ◽

Gouwerok ◽

Veldman ◽

de Korte

Keyword(s):

Storage Container ◽

Platelet Storage

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Fatal sepsis associated with a storage container leak permitting platelet contamination with environmental bacteria after pathogen reduction

Transfusion ◽

10.1111/trf.16210 ◽

2020 ◽

Author(s):

Emmanuel A. Fadeyi ◽

Stephen J. Wagner ◽

Corinne Goldberg ◽

Thea Lu ◽

Pampee Young ◽

...

Keyword(s):

Storage Container ◽

Environmental Bacteria ◽

Pathogen Reduction ◽

Fatal Sepsis

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Loss of Thrombin-Induced Ca2+ Mobilization in a Subpopulation of Platelets during Storage

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646419 ◽

1991 ◽

Vol 66 (03) ◽

pp. 350-354 ◽

Cited By ~ 5

Author(s):

Rob Fijnheer ◽

Christa H E Homburg ◽

Berend Hooibrink ◽

Martine N Boomgaard ◽

Dirk de Korte ◽

...

Keyword(s):

Human Platelets ◽

Flow Cytometer ◽

Maximal Concentration ◽

Gradual Decline ◽

Platelet Storage ◽

Functional Defect ◽

Total Fluorescence ◽

Induced Changes

SummaryThrombin-induced changes in cytosolic free Ca2+ ([Ca2+]i) were studied in human platelets that had been stored for up to 6 days. Changes in [Ca2+]i were measured with Indo-1-loaded platelets and quantitated with two different methods: (i) measurement of the changes in total fluorescence; (ii) measurement of the [Ca2+]i changes in individual platelets in a flow cytometer, allowing the detection of non-responding platelets. The maximal concentration of [Ca2+]i after stimulation with 0.5 U of thrombin/ml decreased from 544 ± 58 nM (mean ± SEM, n = 6) on day 0, to 276 ± 9 nM on day 3 and to 203 ± 23 nM on day 6. The percentage of platelets responding to 0.5 U of thrombin/ml declined from 90 ± 2% on day 0 to 72 ± 4% on day 3, and to 47 ± 8% on day 6. Nevertheless, also the responding platelets showed a decreased rise in [Ca2+]i.The study shows that during platelet storage a decrease in the rise in [Ca2+]i upon thrombin stimulation occurs. This decrease is partly due to the formation of a subpopulation of platelets that is completely unresponsive and partly due to a decreased responsiveness in the remainder of the platelets; it is not due to a gradual decline in [Ca2+]i rise in all platelets. This phenomenon provides new insight in the functional defect of stored platelets.

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Correlation Between Noradrenaline Fluxes, Metabolism and Compartmentalisation in Human Platelets

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657217 ◽

1982 ◽

Vol 48 (01) ◽

pp. 062-066 ◽

Cited By ~ 5

Author(s):

Chantal Legrand ◽

Véronique Dubernard ◽

Philippe Meyer

Keyword(s):

Noradrenaline Release ◽

Human Platelets ◽

Release Of Noradrenaline ◽

Storage Pool ◽

Platelet Storage ◽

Efflux Of Noradrenaline ◽

Preferential Localization

Summary(3H) noradrenaline was taken up by human platelets and partially converted into sulfoconjugated noradrenaline. This uptake was inhibited by drugs which have been previously shown to impair the uptake of 5-HT (ouabain, chlorimipramine) or the storage of 5-HT (tyramine, reserpine) by platelets. In addition, tyramine and reserpine stimulated the formation of sulfoconjugated noradrenaline. The efflux of noradrenaline from platelets was measured in parallel and was found to be directly related to the proportion of non metabolized to metabolized noradrenaline in the cells. Unlike tyramine, which induced a similar release of noradrenaline and 5-HT, reserpine was less effective at inducing noradrenaline release than 5-HT release. This study indicates a preferential localization of noradrenaline in the granular pool of human platelets with the existence of an extragranular sulfoconjugated pool which is increased when the granular storage of noradrenaline is impaired. Studies of noradrenaline fluxes and metabolism may be useful in the understanding of both acquired and inherited platelet storage pool defects.

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