scholarly journals Simultaneous 51CR AND 14C-Serotonin Platelet Survival Measurements

1977 ◽  
Author(s):  
S. Hanson ◽  
L.A. Harker
Keyword(s):  
Arachidonic Acid ◽  
Factor Viii ◽  
Air Bubbles ◽  
Platelet Destruction ◽  
Platelet Survival ◽  
Platelet Release ◽  
Survival Studies ◽  
Bovine Factor

In vivo platelet reactions resulting in platelet utilization or release of constituents without platelet destruction have been studied in baboons by measuring isotopic disappearance of doubly labeled platelets using 51Cr as the cytoplasmic label to detect destruction and 14C-serotonin as a granular |abel to detect release. In 25 normal animals, the 14C-serotonin platelet survival (14C-SPS) was 6.0 days ± 0.2 compared with a Cr platelet survival (51Cr-PS) of 5.5 days ± 0.2, suggesting about 10% reutilization of the 14C label. Platelet labeling in vivo with 51C-serotonin showed that only 13% ± 2% of the injected activity became platelet bound; the remainder was cleared from the plasma within three hours. The platelets labeled in vivo survived normally (6.0 days ± 0.4). These results indicale that in vivo reutilization of serotonin is not extensive and that the process of labeling platelets with Cr in vitro does not appreciably shorten their survival in vivo. In other studies, animals with doubly labeled platelets received intravenous infusions of thrombin, ionophore R02-2985, arachidonic acid, ADP, collagen, plasmin, streptokinase, endotoxin, bovine factor VIII, and air bubbles. Thrombin or collagen infusions produced rapid, equivalent disappearance of both labels that correlated closely with decreases in platelet counts indicating that platelet destruction is not associated with reuptake of released C-serotonin by ambient circulating platelets. In contrast the infusions of R1I2-2985, plasmin or some studies with endotoxin induced selective disappearance of 51C-serotonin while 51Cr-PS was normal, reflecting platelet release in vivo without platelet destruction. With ADP, arachidonic acid, streptokinase and air bubbles platelets disappeared from the circulation transiently without loss of either label indicating transient platelet sequestration. We conclude that doubly labeled platelet survival studies are useful in characterizing platelet reactions and their pharmacologic alterations in vivo.

IN VIVO STUDIES ON RED CELLS AND PLATELETS STORED IN HALFSTRENGTH CITRATE

1987 ◽  
Author(s):  
C Prewse ◽  
K Bell ◽  
B Griffin
Keyword(s):  
Factor Viii ◽  
Coagulation Factor ◽  
Red Cells ◽  
In Vivo Studies ◽  
Dramatic Improvement ◽  
Half Strength ◽  
Survival Studies ◽  
Cellular Components

We have previously shown that donation of blood into anticoagulants containing half the normal amount of citrate results in a dramatic improvement in the stability of coagulation factor VIII and has no adverse effect on the in vitro qualities of red cells or platelets during storage. To confirm the viability of stored cellular components we are now performing autologous survival studies in healthy volunteers using radiolabelled cells from red cells and platelets stored for 35 and 5 days respectively. Results to date indicate a 24 hour survival of 80% for red cells stored at a haematocrit of 0.70 for 35 days. Infusion of Ill-In oxine labelled platelets after storage for 5 days in full or half-strength citrate gave recoveries of 40% and survivals of 7 days. These encouraging results suggest use of halfstrength citrate may be a route to increasing factor VIII supply without any additional donor recruitment. Further in vitro studies have also been performed on cellular components and reveal adequate in vitro quality for half-strength citrate blood held at room temperature for 20 hours prior to component preparation.

INDIUM-111 PLATELET SURVIVAL STUDIES ON PLATELET CONCENTRATES (PCVSTORED FOR UP TO 14 DAYS

1987 ◽  
Author(s):  
S Holme ◽  
W A Heaton ◽  
P Hartman
Keyword(s):  
Survival Data ◽  
In Vitro Assays ◽  
Coefficient Of Determination ◽  
Gamma Model ◽  
Storage Duration ◽  
Platelet Survival ◽  
Indium 111 ◽  
Survival Studies

The effect of extended storage on platelet in vitro and in vivo viability was investigated to determine the reliability and efficacy of Indium-111-oxine radiolabeling of long-term stored platelets. The fitness of various mathematical models for measurement of platelet survival and recovery was also evaluated.33 CPDA-1 PC were prepared and stored for various periods of time (see below) according to standard blood bank methods. The volume of the PC was adjusted to 65-75 mL to prevent pH fall with extended storage. After storage, samples were taken for in vitro assays and for radiolabeling witn Indium-111-oxine using standardized methods. None of the PC had pH<6.3. Afxer reinfusion of the labeled platelets, samples for measurement of radioactivity were taken at three hours and daily for seven days.The uptake {%) of Indium-111 and loss of platelets during the labeling showed no correlation with storage time; the means of the 33 studies were 71±8% and 35±6%, respectively. There was no significant correlation between the parameters and recovery or survival which suggests reliable labeling of nonviable platelets. Excellent fit of the survival data to the multiple hit gamma model was found forpall studies as determined by the coefficient of determination, r 2. The survival curves of platelets stored for one and five days were quite linear as shown by r2 ; with longer storage periods they became more exponential as shown by an increasingly better fit (r2 ) to the log model.Using the gamma model, both in vivo recovery and survival showed a progressive loss with increasing storage duration. This was less evident with the linear model. The loss of in vivo viability paralleled closely a decrease in the in vitro , parameters of platelet quality (discoid shape, hypotonic shock response, ATP content, and oxygen consumption) during storage.In conclusion, this study indicates that extended storage not only yields platelets with reduced recovery, but also platelets with shortened survival.

scholarly journals Platelet von Willebrand's antigen II: active release by aggregating agents and a marker of platelet release reaction in vivo

Blood ◽  
1981 ◽  
Vol 58 (6) ◽  
pp. 1075-1080 ◽  
Author(s):  
JP Scott ◽  
RR Montgomery
Keyword(s):  
Factor Viii ◽  
Adenosine Diphosphate ◽  
Metabolic Inhibitors ◽  
Active Process ◽  
Platelet Destruction ◽  
Platelet Antigen ◽  
Clinical Syndromes ◽  
Platelet Release ◽  
Active Release

von Willebrand's antigen II (vW AgII), a plasma and platelet antigen immunologically and biochemically distinct from factor-VIII-related antigen (VIIIR:Ag), is decreased in von Willebrand's disease. vW AgII is released from platelets during aggregation and clotting. The release of platelet vW AgII was studied in washed platelets following aggregation by thrombin, collagen, and adenosine diphosphate (ADP). Total platelet vW AgII was 3.39 U/10(9) platelets. Thrombin and collagen yielded release of 85% and 86% of platelet vW AgII, respectively, at the highest concentrations. Release of platelet vW AgII was correlated with the release of 5-hydroxytryptamine (5HT). Release of vW AgII by collagen and thrombin was inhibited by metabolic inhibitors. In addition, collagen release of vW AgII was inhibited by aspirin. In clinical syndromes associated with intravascular platelet destruction, marked elevations of plasma vW AgII were noted. Thus, vW AgII is released by a metabolically active process from platelets during aggregation. In addition, vW AgII appears to be a marker of intravascular platelet destruction.

scholarly journals Platelet von Willebrand's antigen II: active release by aggregating agents and a marker of platelet release reaction in vivo

Blood ◽  
1981 ◽  
Vol 58 (6) ◽  
pp. 1075-1080 ◽  
Author(s):  
JP Scott ◽  
RR Montgomery
Keyword(s):  
Factor Viii ◽  
Adenosine Diphosphate ◽  
Metabolic Inhibitors ◽  
Active Process ◽  
Platelet Destruction ◽  
Platelet Antigen ◽  
Clinical Syndromes ◽  
Platelet Release ◽  
Active Release

Abstract von Willebrand's antigen II (vW AgII), a plasma and platelet antigen immunologically and biochemically distinct from factor-VIII-related antigen (VIIIR:Ag), is decreased in von Willebrand's disease. vW AgII is released from platelets during aggregation and clotting. The release of platelet vW AgII was studied in washed platelets following aggregation by thrombin, collagen, and adenosine diphosphate (ADP). Total platelet vW AgII was 3.39 U/10(9) platelets. Thrombin and collagen yielded release of 85% and 86% of platelet vW AgII, respectively, at the highest concentrations. Release of platelet vW AgII was correlated with the release of 5-hydroxytryptamine (5HT). Release of vW AgII by collagen and thrombin was inhibited by metabolic inhibitors. In addition, collagen release of vW AgII was inhibited by aspirin. In clinical syndromes associated with intravascular platelet destruction, marked elevations of plasma vW AgII were noted. Thus, vW AgII is released by a metabolically active process from platelets during aggregation. In addition, vW AgII appears to be a marker of intravascular platelet destruction.

Purification of the Antihemophilic Factor by Gel Filtration on Agarose

1969 ◽  
Vol 22 (03) ◽  
pp. 577-583 ◽  
Author(s):  
M.M.P Paulssen ◽  
A.C.M.G.B Wouterlood ◽  
H.L.M.A Scheffers
Keyword(s):  
Factor Viii ◽  
Plasma Proteins ◽  
Large Scale ◽  
Gel Filtration ◽  
Large Scale Preparation ◽  
Scale Preparation ◽  
Antihemophilic Factor

SummaryFactor VIII can be isolated from plasma proteins, including fibrinogen by chromatography on agarose. The best results were obtained with Sepharose 6B. Large scale preparation is also possible when cryoprecipitate is separated by chromatography. In most fractions containing factor VIII a turbidity is observed which may be due to the presence of chylomicrons.The purified factor VIII was active in vivo as well as in vitro.

Acquired Haemophilia: Functional Study of Antibodies to Factor VIII

1981 ◽  
Vol 45 (03) ◽  
pp. 285-289 ◽  
Author(s):  
J P Allain ◽  
A Gaillandre ◽  
D Frommel
Keyword(s):  
Factor Viii ◽  
Functional Study ◽  
Factor Viii Inhibitor ◽  
Acquired Haemophilia ◽  
Viii Inhibitor ◽  
Kinetics Of ◽  
Antibody Function ◽  
Native Plasma

SummaryFactor VIII complex and its interaction with antibodies to factor VIII have been studied in 17 non-haemophilic patients with factor VIII inhibitor. Low VIII:C and high VIIIR.Ag levels were found in all patients. VIII:WF levels were 50% of those of VTIIRrAg, possibly related to an increase of poorly aggregated and electrophoretically fast moving VIIIR:Ag oligomers.Antibody function has been characterized by kinetics of VIII :C inactivation, saturability by normal plasma and the slope of the affinity curve. Two major patterns were observed:1) Antibodies from 6 patients behaved similarly to those from haemophiliacs by showing second order inhibition kinetics, easy saturability and steep affinity slope (> 1).2) Antibodies from other patients, usually with lower titres, inactivated VIII :C according to complex order kinetics, were not saturable, and had a less steep affinity slope (< 0.7). In native plasma, or after mixing with factor VIII concentrate, antibodies of the second group did not form immune complexes with the whole factor VIII molecular complex. However, dissociation procedures did release some antibodies from apparently low molecular weight complexes formed in vivo or in vitro. For appropriate management of non-haemophilic patients with factor VIII inhibitor, it is important to determine the functional properties of their antibodies to factor VIII.

The Natural Course of Defibrination Syndrome Caused by Echis Colorata Venom in Man

1974 ◽  
Vol 31 (03) ◽  
pp. 420-428 ◽  
Author(s):  
M Fainaru ◽  
S Eisenberg ◽  
N Manny ◽  
C Hershko
Keyword(s):  
Factor Viii ◽  
Blood Coagulation ◽  
Major Bleeding ◽  
Renal Damage ◽  
Specific Treatment ◽  
Natural Course ◽  
Factor V ◽  
Thrombocyte Count

SummaryThe natural course of defibrination syndrome caused by Echis colorata venom (ECV) in five patients is reported. All patients developed afibrinogenemia within six hours after the bite. Concomitantly a depression in factor V was recorded. Factor VIII and thrombocyte count in blood were normal in most patients. In the light of the known effects of ECV on blood coagulation in vivo and in vitro it is concluded that the afibrinogenemia is due to intravascular clotting.Four patients had transient renal damage, manifested by oliguria, azotemia, albuminuria and cylindruria, ascribed to microthrombi in the renal glomeruli.After the bite, the natural course was benign, no major bleeding was observed, and all signs of coagulopathy reverted to normal within 7 days. Therefore we recommend no specific treatment for this condition. In the case of heavily bleeding patients, administration of antiserum against ECV and/or heparin should be considered.

Comparison of the Actions of Thrombin and the Thrombin-Like Venom Enzymes Ancrod and Batroxobin

1976 ◽  
Vol 36 (01) ◽  
pp. 009-013 ◽  
Author(s):  
D. L Aronson
Keyword(s):  
Factor Viii ◽  
Fibrinopeptide A ◽  
Enzymic Reaction

SummaryThrombin acts on several coagulant proteins to produce products with physiologic, pharmacologic and pathologic potential. The most sensitive thrombin substrate seems to be factor VIII. Some thrombin dependent reactions studied in vitro and proposed as control reactions seem too insensitive to the action of thrombin to be of in vivo significance.The only enzymic reaction the thrombin-like venom enzymes, Ancrod and Batroxobin, have in common with thrombin is the removal of fibrinopeptide A.

The Development of Homologous (Canine/Anti-Canine) Antibodies in Dogs with Haemophilia A (Factor VIII Deficiency): A Ten-Year Longitudinal Study

1993 ◽  
Vol 69 (01) ◽  
pp. 021-024 ◽  
Author(s):  
Shawn Tinlin ◽  
Sandra Webster ◽  
Alan R Giles
Keyword(s):  
Factor Viii ◽  
Canine Model ◽  
Significant Inhibition ◽  
Human Condition ◽  
Haemophilia A ◽  
Variable Expression ◽  
The Family ◽  
Over Time

SummaryThe development of inhibitors to factor VIII in patients with haemophilia A remains as a serious complication of replacement therapy. An apparently analogous condition has been described in a canine model of haemophilia A (Giles et al., Blood 1984; 63:451). These animals and their relatives have now been followed for 10 years. The observation that the propensity for inhibitor development was not related to the ancestral factor VIII gene has been confirmed by the demonstration of vertical transmission through three generations of the segment of the family related to a normal (non-carrier) female that was introduced for breeding purposes. Haemophilic animals unrelated to this animal have not developed functionally significant factor VIII inhibitors despite intensive factor VIII replacement. Two animals have shown occasional laboratory evidence of factor VIII inhibition but this has not been translated into clinical significant inhibition in vivo as assessed by clinical response and F.VIII recovery and survival characteristics. Substantial heterogeneity of inhibitor expression both in vitro and in vivo has been observed between animals and in individual animals over time. Spontaneous loss of inhibitors has been observed without any therapies designed to induce tolerance, etc., being instituted. There is also phenotypic evidence of polyclonality of the immune response with variable expression over time in a given animal. These observations may have relevance to the human condition both in determining the pathogenetic factors involved in this condition and in highlighting the heterogeneity of its expression which suggests the need for caution in the interpretation of the outcome of interventions designed to modulate inhibitor activity.

Factor-VIII Inhibitor in Less Severely Affected Haemophilic Patients

1975 ◽  
Author(s):  
E. G. D. Tuddenham ◽  
A. L. Bloom ◽  
J. C. Giddings ◽  
C. A. Barrett
Keyword(s):  
Factor Viii ◽  
Factor Viii Inhibitor ◽  
Factor Viii Level ◽  
Replacement Treatment ◽  
Viii Level ◽  
Viii Inhibitor ◽  
In Vivo Recovery ◽  
Better Than

The occurrence of factor VIII inhibitor in five mild or moderately affected liaemophilic patients is described. In four patients the inhibitor inactivated endogenous factor VIII an dtemporarily converted them to severely affected haemophiliacs with factor VIII level of 0%. In the fifth patient, a brother of one of the others, the inhibitor although more potent did not inactivate the patient’s own factor VIII and did not completely inactivate normal factor VIII in vitro. This patient responded to treatment with factor-VIII concentrate but the in-vivo recovery was reduced. The patient’s plasma was tested against a panel of normal donors but it inactivated factor VIII in each to a similar extent and no evidence for normal factor-VIII groups was obtained. In the other patients the response to replacement treatment was also better than that usually seen in severely affected haemophilic patients with inhibitor. In the two related patients the inhibitors have so far persisted but in the unrelated patients the inhibitors eventually disappeared and did not always recur with subsequent therapy. The incidence of factor- VIII inhibitor in less severe haemophiliacs (factor VIII > 3% ) in this centre is 6% suggesting that the complication is more frequent in this type of patient than hitherto recognised.

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