T2 Magnetic Resonance to Monitor Hemostasis

2018 ◽  
Vol 45 (03) ◽  
pp. 247-252 ◽  
Author(s):  
Adam Cuker ◽  
Joseph Marturano ◽  
Maria Carinato ◽  
Thomas Lowery ◽  
Douglas Cines

AbstractThere is a clinical need for pragmatic approaches to measure integrated hemostatic reactions in whole blood rapidly, using small volumes of blood. The authors have applied T2 magnetic resonance (T2MR) to assess coagulation reactions based on partitioning of red blood cells and proteins that occurs during fibrin formation and platelet-mediated clot contraction. T2MR is amenable to measuring clotting times, individual coagulation factors, and platelet function. T2MR also revealed a novel “hypercoagulable” signature characterized by fibrin clots almost insusceptible to fibrinolysis that surround tessellated arrays of polyhedral erythrocytes (“third peak”). This signature, which develops under conditions associated with intense clot formation in vitro, may help identify patients at risk of developing thrombosis and for monitoring antithrombotic therapies in the future.

2014 ◽  
Vol 111 (03) ◽  
pp. 447-457 ◽  
Author(s):  
Marisa Ninivaggi ◽  
Gerhardus Kuiper ◽  
Marco Marcus ◽  
Hugo ten Cate ◽  
Marcus Lancé ◽  
...  

SummaryBlood dilution after transfusion fluids leads to diminished coagulant activity monitored by rotational thromboelastometry, assessing elastic fibrin clot formation, or by thrombin generation testing. We aimed to determine the contributions of blood cells (platelets, red blood cells) and plasma factors (fibrinogen, prothrombin complex concentrate) to fibrin clot formation under conditions of haemodilution in vitro or in vivo. Whole blood or plasma diluted in vitro was supplemented with platelets, red cells, fibrinogen or prothrombin complex concentrate (PCC). Thromboelastometry was measured in whole blood as well as plasma; thrombin generation was determined in parallel. Similar tests were performed with blood from 48 patients, obtained before and after massive fluid infusion during cardiothoracic surgery. Addition of platelets or fibrinogen, in additive and independent ways, reversed the impaired fibrin clot formation (thromboelastometry) in diluted whole blood. In contrast, supplementation of red blood cells or prothrombin complex concentrate was ineffective. Platelets and fibrinogen independently restored clot formation in diluted plasma, resulting in thromboelastometry curves approaching those in whole blood. In whole blood from patients undergoing dilution during surgery, elastic clot formation was determined by both the platelet count and the fibrinogen level. Thrombin generation in diluted (patient) plasma was not changed by fibrinogen, but improved markedly by prothrombin complex concentrate. In conclusion, in dilutional coagulopathy, platelets and fibrinogen, but not red blood cells or vitamin K-dependent coagulation factors, independently determine thromboelastometry parameters measured in whole blood and plasma. Clinical decisions for transfusion based on thromboelastometry should take into account the platelet concentration.


1958 ◽  
Vol 193 (2) ◽  
pp. 244-248 ◽  
Author(s):  
Perry Ruth Stahl ◽  
Homer E. Dale

In a repeated study on 17 dairy calves, T-1824 dye plasma dilution showed significantly higher blood volumes than were found by any other technique or computation method using Cr51-tagged red blood cells. Five blood samples taken at 20-minute intervals after injection showed consistent decrease in radioactivity count from the first to the last sample, indicating greater accuracy in radioactivity dilution regressed to zero time figures than in average counts of several postinjection samples. In vitro studies suggest a loss of Cr51 from red blood cells to plasma after saline washings are Cr-free. Percentage blood volumes computed from whole blood samples of calves injected with Cr51-tagged red blood cells decreased in a straight line relationship with increase of body weight. Percentage plasma and whole blood volumes estimated with the T-1824 dye technique decreased regularly with body weight increase until a second determination was made when there was a rapid rise nearly to the level of the smallest calves, followed by another regular decrease with increase in weight. It is suggested that repeated dye injections do not always measure the same space. Regressed values of five whole blood samples taken at 20-minute intervals after injection of Cr51 tagged red blood cells gave more consistent blood volume determinations than either the weighed red cells or the plasma dye dilutions of the same samples.


Biologicals ◽  
2010 ◽  
Vol 38 (1) ◽  
pp. 14-19 ◽  
Author(s):  
N.A. Mufti ◽  
A.C. Erickson ◽  
A.K. North ◽  
D. Hanson ◽  
L. Sawyer ◽  
...  

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 986-986
Author(s):  
Alison Leigh Banka ◽  
Mark Shamoun ◽  
Mario Gutierrez ◽  
Tyler Tanski ◽  
Lola Eniola-Adefeso

Introduction: Sickle cell disease (SCD) occurs due to a mutation in the β-subunit of hemoglobin, causing stiffening of red blood cells (RBCs) and leading to RBC sickling and vaso-occlusive crises (VOC) in SCD patients. While sickled RBCs remain a hallmark of SCD, they are prone to lysis and represent a small fraction of the total RBCs present in patients at a given time. The remaining RBCs maintain a normal, discoid shape and are either healthy or stiff due to polymerization of the hemoglobin β-globin subunit. In healthy blood flow, RBCs form a core in the center of the vessel and the remaining cells, platelets and white blood cells (WBCs), marginate towards the endothelium. However, the increased stiffness of RBCs in SCD disrupts this neat segregation of blood cells to different areas of the blood vessel and can contribute to VOC, the root cause of many acute and chronic complications for SCD patients. Despite the presence of normally shaped, stiffened RBCs in SCD patients, the impact of these RBCs on other cell types in blood flow is currently not well understood. Our laboratory previously demonstrated that the presence of artificially rigidified RBCs leads to an expansion of the RBC core and significantly decreases WBC adhesion to an inflamed endothelium in vitro. Here, we examine the impact of stiffened RBCs on platelet adhesion to a damaged endothelium in vitro by first using a model system with artificially rigidified RBCs and second, utilizing SCD patient blood to further support our model and understand platelet-RBC interactions in SCD patients. Methods: In our model system, we artificially rigidified RBCs taken from healthy donors and reconstituted them into whole blood before perfusing the mixture over an activated, damaged endothelium using a parallel plate flow chamber. We quantified platelet adhesion to the endothelium in comparison to healthy, non-rigidified controls using fluorescent microscopy. To determine if our model findings translated to SCD, we recruited a cohort of hemoglobin SS and SC patients during routine visits and similarly perfused their whole blood over the same damaged endothelium and quantified platelet adhesion. Results and conclusions: The inclusion of artificially rigidified RBCs in otherwise healthy subject blood flow significantly increased platelet adhesion to a damaged endothelium with a maximum increase in platelet adhesion of six-fold over a healthy, non-rigid control in our model system. Both RBC rigidity and the percentage of RBCs that were artificially rigidified had a large impact on the increase in platelet adhesion. SCD platelet adhesion to the damaged endothelium model varied from donor to donor based on variables such as treatment method and disease severity. Overall, this work experimentally elucidates the biophysical impact of stiffened RBCs on platelet adhesion using both an artificial model utilizing healthy blood as well as SCD blood, which can help determine the mechanism of action causing VOC in SCD. Disclosures No relevant conflicts of interest to declare.


Transfusion ◽  
2019 ◽  
Vol 59 (10) ◽  
pp. 3197-3204
Author(s):  
Peter Schubert ◽  
Brankica Culibrk ◽  
Deborah Chen ◽  
Katherine Serrano ◽  
Elena Levin ◽  
...  

Transfusion ◽  
2013 ◽  
Vol 54 (6) ◽  
pp. 1569-1579 ◽  
Author(s):  
Sherry L. Spinelli ◽  
Katie L. Lannan ◽  
Ann E. Casey ◽  
Amanda Croasdell ◽  
Timothy M. Curran ◽  
...  

1987 ◽  
Author(s):  
C L Balduini ◽  
G Bertolino ◽  
G Polino ◽  
G Gamba ◽  
F Sinigaglia ◽  
...  

We investigated the effect of red blood cells (RBC) on "in vitro" platelet aggregation by the use of the "Electronic Whole Blood Aggregometer" (Chrono-Log Corporation). Preliminary experiments, studying platelet aggregation in the same PRP by the simultaneous use of the optical method and the electronic method, demonstrated that the maximum rate of impedance changes corre lated well with both the rate and the extent of platelet aggregation as measured by the optical method. The refore, the maximum rate of impedance increase was cho sen for the measurement of platelet aggregation in the presence of different concentrations of RBC. RBC, both at 40 and 60%, significantly inhibited platelet aggregation stimulated by low and high concentration of ADP and epinephrine. Platelet aggregation stimulated by co llagen was slightly reduced only by the higher RBC con centration. The effect of RBC on platelet aggregation was also investigated in idiopathic myelofibrosis, a pathological condition characterized by both platelet and RBC alterations. While on the basis of PRP studies 5 out of 17 patients had hypo-aggregation and 12 had normal aggregation, whole blood studies evidentiated hypo-aggregation in 3 patients, normal aggregation in 4 and spontaneous platelet aggregation (SPA) in 10. SPA was a consequence of platelet abnormality, since it occurred also when platelets from patients were sti rred with normal RBC.In conclusion, RBC may exert different effects on the aggregation of normal and pathological platelets.


Blood ◽  
1950 ◽  
Vol 5 (2) ◽  
pp. 129-147 ◽  
Author(s):  
WILLIAM DAMESHEK ◽  
JACOB NEBER

Abstract 1. The clinical histories of 11 patients with a severe and hitherto undescribed type of reaction to in vitro compatible whole blood are presented. These patients all experienced beneficial responses to therapy with washed red blood cell transfusions. The technic of washing the blood is outlined. 2. In 5 of the patients, sensitivity to a heat-labile constituent of fresh normal plasma was demonstrated. In the remaining 6 patients, although actual sensitivity to plasma was not proved, transfusions of washed red blood cells were well tolerated and were therapeutically effective. 3. These uncommon reactions to the plasma in whole blood are differentiated from the usual pyrogenic, allergic or hemolytic plasma reactions by their ease of repetition in the absence of pyrogens, by lack of the usual allergic manifestations, and by the failure to demonstrate hemoglobinemia or hemoglobinuria. 4. A simple diagnostic test ("plasma provocative test") is described which appears to be of specific value in the differentiation of the reaction. 5. It is suggested that in any instance of severe transfusion reaction to apparently compatible whole blood this type of sensitivity to the donated plasma should be borne in mind as a possible cause. The plasma provocative test should then be tried. If positive, the transfusion of well washed red blood cells will probably be effective and in some cases may be of life-saving importance.


1992 ◽  
Vol 173 (1) ◽  
pp. 25-41 ◽  
Author(s):  
R. A. Ferguson ◽  
N. Sehdev ◽  
B. Bagatto ◽  
B. L. Tufts

In vitro experiments were carried out to examine the interactions between oxygen and carbon dioxide transport in the blood of the sea lamprey. Oxygen dissociation curves for whole blood obtained from quiescent lampreys had Hill numbers (nH) ranging from 1.52 to 1.89. The Bohr coefficient for whole blood was -0.17 when extracellular pH (pHe) was considered, but was much greater (-0.63) when red blood cell pH (pHi) was considered. The pHi was largely dependent on haemoglobin oxygen- saturation (SO2) and the pH gradient across the red blood cell membrane was often reversed when PCO2 was increased and/or SO2 was lowered. The magnitude of the increase in pHi associated with the Haldane effect ranged from 0.169 pH units at 2.9 kPa PCO2 to 0.453 pH units at a PCO2 of 0.2 kPa. Deoxygenated red blood cells had a much greater total CO2 concentration (CCO2) than oxygenated red blood cells, but the nonbicarbonate buffer value for the red blood cells was unaffected by oxygenation. Plasma CCO2 was not significantly different under oxygenated or deoxygenated conditions. Partitioning of CO2 carriage in oxygenated and deoxygenated blood supports recent in vivo observations that red blood cell CO2 carriage can account for much of the CCO2 difference between arterial and venous blood. Together, the results also suggest that oxygen and carbon dioxide transport may not be tightly coupled in the blood of these primitive vertebrates. Finally, red cell sodium concentrations were dependent on oxygen and carbon dioxide tensions in the blood, suggesting that sodium-dependent ion transport processes may contribute to the unique strategy for gas transport in sea lamprey blood.


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