Sodium citrate tubes

Manufactured by Sarstedt

Sourced in Germany

Sodium citrate tubes are laboratory equipment used for the collection and storage of blood samples. They contain sodium citrate, which acts as an anticoagulant, preventing the blood from clotting during sample processing and analysis.

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Lab products found in correlation

Z2 particle counter, by Beckman Coulter (1 mentions) Prostaglandin e1, by Merck Group (1 mentions) Anti cd45 microbeads, by Miltenyi Biotec (1 mentions) Acl top 700, by Werfen (1 mentions)

Close spelling variants of this product

Citrate tubes Sodium citrate

6 protocols using sodium citrate tubes

Murine Platelet Isolation and Activation

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Blood was obtained by cardiac puncture from mice anesthetized with 2% isoflurane (Vetfluorane^®, Virbac), and collected into sodium citrate tubes (Sarstedt, Germany). Platelet rich plasma (PRP) was prepared from anticoagulated blood by double centrifugation at 100 × g for 4 and 5 min, respectively. Platelets were pelleted by centrifuging PRP at 1300 × g for 5 min and resuspended in Tyrode’s Hepes Buffer (134 mM NaCl, 0.34 mM Na₂HPO₄, 2.9 mM KCl, 12 mM NaHCO₃, 20 mM HEPES [pH 7.4] and 5 mM glucose) and allowed to rest at RT for at least 30 min. After isolation, platelet number was equalized using Beckman Coulter Z2 particle counter.
Platelets were stimulated with the indicated agonists and conditions, depending on the assay. Platelet activation was determined by flow cytometry via measuring the high-affinity conformation of the integrin αIIbβ3 and the exposure of P-selectin after treatment with PKC inhibitors, as described [3 (link)].

Fernández-Infante C., Hernández-Cano L., Herranz Ó., Berrocal P., Sicilia-Navarro C., González-Porras J.R., Bastida J.M., Porras A, & Guerrero C. (2024). Platelet C3G: a key player in vesicle exocytosis, spreading and clot retraction. Cellular and Molecular Life Sciences: CMLS, 81(1), 84.

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Platelet Isolation and Activation Protocol

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Blood was drawn into sodium citrate tubes (Sarstedt) and centrifuged at 170g for 10 min at room temperature to obtain platelet‐rich plasma. Platelet‐rich plasma was supplemented with prostaglandin E1 (1 μM; Sigma Aldrich) and centrifuged at 900g for 5 min. The platelet pellet was resuspended in wash buffer (10 mM sodium citrate, 1% w/v dextrose, 150 mM NaCl, pH 7.4). Subsequently, platelets were centrifuged for 5 min at 720g, supernatant was removed, and the platelet pellet was resuspended in Tyrode's buffer (134 mM NaCl, 12 mM NaHCO₃, 2.9 mM KCl, 0.34 mM Na₂HPO₄, 1 mM MgCl₂, 10 mM HEPES, pH 7.4) containing 5 mM dextrose and 0.5 U/ml apyrase. Platelets were recalcified to 1.8 mM CaCl₂ after 15–30 min.

Dhami S.P., Patmore S., Comerford C., Byrne C.M., Cavanagh B., Castle J., Kirwan C.C., Kenny M., Schoen I., O'Donnell J.S, & O'Sullivan J.M. (2022). Breast cancer cells mediate endothelial cell activation, promoting von Willebrand factor release, tumor adhesion, and transendothelial migration. Journal of Thrombosis and Haemostasis, 20(10), 2350-2365.

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Immune Cell Fractionation and Genomic Analysis

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Peripheral blood (20 mL) was collected in sodium citrate tubes (Sarstedt, Nümbrecht, Germany). PBMNC were isolated by density gradient centrifugation. The median enrichment of WBC by density gradient centrifugation was approximately threefold. EpCAM-positive cells and CD45-negative cells were enriched in two parallel reactions using anti-EpCAM (CD326) and anti-CD45 microbeads (Miltenyi Biotech, Bergisch Gladbach, Germany). Genomic DNA was isolated from the resulting four sample fractions (CD45⁺, CD45⁻, CD326⁺ and CD326⁻) and subjected to real time-PCR and melting curve analysis.

Breitenbuecher F., Hoffarth S., Worm K., Cortes-Incio D., Gauler T.C., Köhler J., Herold T., Schmid K.W., Freitag L., Kasper S, & Schuler M. (2014). Development of a Highly Sensitive and Specific Method for Detection of Circulating Tumor Cells Harboring Somatic Mutations in Non-Small-Cell Lung Cancer Patients. PLoS ONE, 9(1), e85350.

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Platelet Isolation from Healthy Donors

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Human platelets were obtained from healthy volunteers. Donors did not use non-steroidal anti-inflammatory drugs for at least 10 days. Venous whole blood was collected into 3.2% sodium citrate tubes (Sarstedt, Nümbercht, Germany). The study was approved by the local Ethics Committee (Universitätsklinikum Regensburg, Ethikkommission der medizinischen Fakultät, proposal 17-696-101). All subjects had given their informed consent to participate in the study. All research was performed in accordance with the relevant guidelines and regulations.

Heimerl S., Höring M., Kopczynski D., Sigruener A., Hart C., Burkhardt R., Black A., Ahrends R, & Liebisch G. (2023). Quantification of bulk lipid species in human platelets and their thrombin-induced release. Scientific Reports, 13, 6154.

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Anticoagulant Monitoring: Bedside and Lab Tests

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Bedside POCT of PT/INR, aPTT and ACT was conducted from whole blood. ACT was measured using ACT plus (ACT+) and ACT-low range (ACT-LR) test cards that contain different reagents and cover different measurement ranges. Further samples were collected in 3.2% sodium-citrate tubes (Sarstedt, Nümbrecht, Germany), and instantly centrifuged to acquire plasma. Laboratory-based anti-Xa activity was measured using Chromogenix COAMATIC Heparin Test on an ACL TOP 700 (Instrumentation Laboratory, Kirchheim, Germany). TECHNOVIEW calibrators (Technoclone, Vienna, Austria) were used to determine apixaban and rivaroxaban concentrations with limits of quantification of 10 and 18 ng/mL. Remaining plasma aliquots were stored at –80 °C until testing of diluted thrombin time (dTT; Hemoclot assay, Hyphen BioMed, Neuville-sur-Oise, France). As the gold standard, DOAC concentrations were determined by ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS) [8 (link)]. All coagulation testing was performed according to manufacturers’ instructions by thoroughly trained investigators and technicians.

Ebner M., Birschmann I., Peter A., Spencer C., Härtig F., Kuhn J., Blumenstock G., Zuern C.S., Ziemann U, & Poli S. (2017). Point-of-care testing for emergency assessment of coagulation in patients treated with direct oral anticoagulants. Critical Care, 21, 32.

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Platelet-poor Plasma Preparation

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Venous blood was drawn without stasis onto 3.2% sodium citrate tubes (1 part of citrate to 9 parts of blood; SARSTEDT AG&Co., Nümbrecht, Germany), and blood samples were centrifuged at 2500×g for 10 min within 30 min to prepare platelet-poor plasma. In a follow-up study, plasma was taken from a patient with PE prior to treatment with LMWH, which was subsequently centrifuged twice at 2500 g for 10 min each time. All plasma samples were aliquoted, immediately frozen, stored at −80 °C, and shipped to the laboratory in Leeds on dry ice. Plasma samples were thawed in a 37 °C water bath for 10 min.

Baker S.R., Halliday G., Ząbczyk M., Alkarithi G., Macrae F.L., Undas A., Hunt B.J, & Ariëns R.A. (2023). Plasma from patients with pulmonary embolism show aggregates that reduce after anticoagulation. Communications Medicine, 3, 12.

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