Platelet Aggregation Following Defibrination with Ancrod

1975 ◽  
Author(s):  
Lawrence C. Slade ◽  
Abe W. Andes
Keyword(s):  
Platelet Aggregation ◽  
Degradation Product ◽  
Intravenous Infusion ◽  
Platelet Response ◽  
Fibrin Degradation Product ◽  
Product Titer ◽  
Inhibition Of Platelet Aggregation ◽  
Normal Platelet ◽  
Maximum Inhibition ◽  
Slow Intravenous Infusion

A transient defect in platelet aggregation was observed following defibrination with Ancrod. Adult mongrel dogs were defibrinated using a slow intravenous infusion of Ancrod. Defibrination was maintained for ninety-six hours. Immediately following defibrination there was a complete ablation of the normal platelet response to thrombin or ADP with a gradual return toward normal aggregation over the ninety-six hour period. Fibrin degradation product titers were highest at the time of maximum inhibition of platelet aggregation. The return to normal aggregation paralleled the fall in the fibrin degradation product titer.

Fibrinogen Proteolysis And Platelet Activation In Myeloproliferative Disorders

1981 ◽  
Author(s):  
H Ireland ◽  
D A Lane ◽  
S Wolff ◽  
G D Pegrum
Keyword(s):  
Platelet Aggregation ◽  
Normal Values ◽  
Plasma Concentrations ◽  
Cell Mass ◽  
Myeloproliferative Disorders ◽  
Secondary Response ◽  
Platelet Response ◽  
Normal Platelet ◽  
Large Platelet ◽  
Red Cell Mass

We have studied 18 patients with myeloproliferative disorders to determine whether their abnormal platelet function and increased plasma β thromboglobulin (β TG) are associated with activated coagulation and fibrinolytic systems. Of these patients, 8 had polycythaemia rubra vera, 8 had myelofibrosis and 2 had thrombocythaemia. We measured plasma concentrations of the thrombin sensitive fragment fibrinopeptide A (FPA), the plasmin sensitive fibrinogen fragment B β1-42, and β TG by radioimmunoassay. We also studied platelet aggregation in response to ADP. Mean normal values (n = 20) for FpA, B β1-42 and βTG were 1.06, 1.59 and 0.80 pmol/ml respectively. The 18 patients showed minimal plasma thrombin and plasmin activities with a disproportionately large platelet release. Mean FpA, B β1-42 and β TG levels were 1.74, 3.31 and 3.12 pmol/ml, respectively. These patients exhibited increased, decreased and normal platelet aggregation but no specific defect was associated with any particular radioimmunoassay result. 5 of these patients, 4 of whom had increased aggregation, were treated with aspirin in sufficient doses to eliminate their secondary response to ADP. FPA and B β1-42 were not altered but β TG was reduced from 3.39 to 2.72 pmol/ml. We also studied 10 patients with idiopathic polycythaemia. These patients showed a normal platelet response to ADP. Their FPA, B β1-42 and β TG levels were similar to normal, 0.7, 1.93 and 0.97 pmol/ml respectively. We conclude that in myeloproliferative disorders (a) the increased plasma concentration of β TG is not associated with a particular platelet aggregation abnormality (b) in the majority of patients the increased β TG level is not a consequence of thrombin action (c) the raised FpA and B β1-42 plasma levels in the minority of patients cannot be attributed solely to increased red cell mass (d) much of the β TG release is probably independent of the cyclooxygenase pathway.

scholarly journals Platelet Receptor Activity for Predicting Survival in Patients with Intracranial Bleeding

2021 ◽  
Vol 10 (10) ◽  
pp. 2205
Author(s):  
Barbara Dragan ◽  
Barbara Adamik ◽  
Malgorzata Burzynska ◽  
Szymon Lukasz Dragan ◽  
Waldemar Gozdzik
Keyword(s):  
Platelet Aggregation ◽  
Function Analysis ◽  
Strong Predictor ◽  
Adenosine Diphosphate ◽  
Intracranial Bleeding ◽  
Rank Test ◽  
Blood Coagulation Disorders ◽  
Platelet Response ◽  
Normal Platelet ◽  
Platelet Receptor

Blood coagulation disorders in patients with intracranial bleeding as a result of head injuries or ruptured aneurysms are a diagnostic and therapeutic problem and appropriate assessments are needed to limit CNS damage and to implement preventive measures. The aim of the study was to monitor changes in platelet aggregation and to assess the importance of platelet dysfunction for predicting survival. Platelet receptor function analysis was performed using the agonists arachidonic acid (ASPI), adenosine diphosphate (ADP), collagen (COL), thrombin receptor activating protein (TRAP), ristocetin (RISTO) upon admission to the ICU and on days 2, 3, and 5. On admission, the ASPI, ADP, COL, TRAP, and RISTO tests indicated there was reduced platelet aggregation, despite there being a normal platelet count. In ‘Non-survivors’, the platelet response to all agonists was suppressed throughout the study period, while in ‘Survivors’ it improved. Measuring platelet function in ICU patients with intracranial bleeding is a strong predictor related to outcome: patients with impaired platelet aggregation had a lower 28-day survival rate compared to patients with normal platelet aggregation (log-rank test p = 0.014). The results indicated that measuring platelet aggregation can be helpful in the early detection, diagnosis, and treatment of bleeding disorders.

Platelet Aggregation Following Defibrination with Ancrod

1976 ◽  
Vol 36 (02) ◽  
pp. 424-429 ◽  
Author(s):  
C Lawrence Slade ◽  
W Abe Andes ◽  
Arthur D. Mason
Keyword(s):  
Platelet Aggregation ◽  
Degradation Product ◽  
Fibrinogen Concentration ◽  
Entire Study Period ◽  
Fibrin Degradation Product ◽  
Entire Study ◽  
Product Level ◽  
Marked Inhibition

Summary In vitro platelet aggregation was studied in dogs following defibrination with Ancrod. There was marked inhibition of aggregation immediately after defibrination. A gradual return toward normal aggregation was observed over the 96 hours study period, but aggregation was still abnormal at 96 hours after defibrination. There was an inverse and highly significant correlation between aggregation and fibrin degradation product level. Fibrinogen was not measurable after defibrination for the entire study period. Aggregation was thus independent of fibrinogen concentration in this study.

THE BLEEDING TENDENCY OF PROGRESSIVE RENAL FAILURE IS NOT ASSOCIATED WITH DEFECTIVE PLATELET AGGREGATION

1987 ◽  
Author(s):  
M P Gordge ◽  
R W Faint ◽  
P B Rylance ◽  
G H Neild
Keyword(s):  
Renal Failure ◽  
Platelet Aggregation ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Plasma Creatinine ◽  
Bleeding Tendency ◽  
Platelet Response ◽  
Normal Platelet ◽  
Von Willebrand ◽  
Induced Aggregation

The bleeding tendency of uraemia may be related to reduction by anaemia of erythrocyte/platelet interaction, toxic inhibition of platelet aggregation and abnormal von Willebrand Factor (vWF) mediated platelet adhesion. Our aim in this study was to determine at what stage of renal failure bleeding time becomes prolonged and to investigate the mechanisms involved.We have measured bleeding time (Simplate II), plasma levels of fibrinogen and vWF, and ex-vivo platelet responsiveness in 31 patients with chronic renal failure (CRF) of various degrees of severity and compared them with values obtained in 22 healthy controls. No patient was dialysed, nephrotic or suffering from immunological renal disease. Patients were divided into mild (plasma creatinine <300 umol/1), n=10, moderate (300-600 umol/1), n=14, or severe (>600 umol/1), n=7, CRF.Bleeding time became significantly prolonged only in severe CRF (p<0.005). Haematocrit fell as renal failure advanced, and correlated with bleeding time (r=0.40, p<0.05). Platelet counts were normal. Platelet aggregation in response to ristocetin (mediated by vWF) and ADP increased progressively (p<0.005 in severe CRF), as did spontaneous aggregation (p<0.005 in severe CRF). This was associated with an increase in plasma vWF and fibrinogen (p<0.005 in severe CRF). Collagen induced aggregation was slightly, but not significantly increased. Thromboxane (TxB2) generation in clotting blood was the only measurement that showed a reduced platelet response (p<0.025 in severe CRF).In summary, a bleeding tendency develops late in the course of progressive CRF when plasma creatinine has risen to at least 600 umol/1. Platelet aggregation is enhanced rather than reduced and platelet interaction with vWF is not defective. Anaemia appears more important than abnormal platelet aggregation in mediating uraemic bleeding, although reduced serum TxB2 generation suggests a defect in platelet response to endogenous thrombin which may also contribute. Increased platelet aggregation and fibrinogen concentrations might promote glomerular thrombosis and contribute to the progression of CRF.

Essential Athrombia

1975 ◽  
Vol 33 (02) ◽  
pp. 278-285 ◽  
Author(s):  
Şeref Inceman ◽  
Yücel Tangün
Keyword(s):  
Platelet Aggregation ◽  
Bleeding Time ◽  
Bleeding Tendency ◽  
Clot Retraction ◽  
Platelet Factor ◽  
Prolonged Bleeding Time ◽  
Normal Platelet ◽  
Aggregation Response ◽  
Platelet Disorder ◽  
Fibrinogen Content

SummaryA constitutional platelet function disorder in a twelve-year-old girl characterized by a lifelong bleeding tendency, prolonged bleeding time, normal platelet count, normal clot retraction, normal platelet factor 3 activity and impaired platelet aggregation was reported.Platelet aggregation, studied turbidimetrically, was absent in the presence of usual doses of ADP (1–4 μM), although a small wave of primary aggregation was obtained by very large ADP concentrations (25–50 μM). The platelets were also unresponsive to epinephrine, thrombin and diluted collagen suspensions. But an almost normal aggregation response occurred with strong collagen suspensions. The platelets responded to Ristocetin. Pelease of platelet ADP was found to be normal by collagen and thrombin, but impaired by kaolin. Platelet fibrinogen content was normal.The present case, investigated with recent methods, confirms the existence of a type of primary functional platelet disorder characterized solely by an aggregation defect, described in 1955 and 1962 under the name of “essential athrombia.”

Responses of Platelets to Strains of Streptococcus sanguis: Findings in Healthy Subjects, Bernard-Soulier, Glanzmann’s, and Collagen-Unresponsive Patients

1987 ◽  
Vol 57 (02) ◽  
pp. 222-225 ◽  
Author(s):  
A H Soberay ◽  
M C Herzberg ◽  
J D Rudney ◽  
H K Nieuwenhuis ◽  
J J Sixma ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Healthy Subjects ◽  
Normal Subjects ◽  
Membrane Glycoprotein ◽  
Response Mechanism ◽  
Platelet Response ◽  
Induce Platelet Aggregation ◽  
Streptococcus Sanguis ◽  
Lag Times ◽  
Bernard Soulier Syndrome

SummaryThe ability of endocarditis and dental strains of Streptococcus sanguis to induce platelet aggregation in plasma (PRP) from normal subjects were examined and compared to responses of PRP with known platelet membrane glycoprotein (GP) and response defects. S. sanguis strains differed in their ability to induce normal PRPs to aggregate. Strains that induced PRP aggregation in more than 60% of donors were significantly faster agonists (mean lag times to onset of aggregation less than 6 min) than those strains inducing response in PRPs of fewer than 60% of donors.Platelets from patients with Bernard-Soulier syndrome aggregated in response to strains of S. sanguis. In contrast, platelets from patients with Glanzmann’s thrombasthenia and from a patient with a specific defect in response to collagen were unresponsive to S. sanguis. These observations show that GPIb and V are not essential, but GPIIb-IIIa and GPIa are important in the platelet response mechanism to S. sanguis. Indeed, the data suggests that the platelet interaction mechanisms of S. sanguis and collagen may be similar.

Some Effects of Fibrinogen Degradation Products (FDP) on Blood Platelets

1966 ◽  
Vol 15 (03/04) ◽  
pp. 413-419 ◽  
Author(s):  
Z Jerushalmy ◽  
M. B Zucker
Keyword(s):  
Platelet Aggregation ◽  
Connective Tissue ◽  
Degradation Products ◽  
Blood Platelets ◽  
Adenosine Diphosphate ◽  
Serotonin Release ◽  
Fibrinogen Degradation Products ◽  
Inhibition Of Platelet Aggregation

Summary“Early” fibrinogen degradation products are more potent inhibitors of thrombin-induced clotting than “late” products and also interfere with the ability of thrombin to release serotonin from platelets. “Early” and “intermediate” FDP cause moderate inhibition of platelet aggregation induced by adenosine diphosphate or connective tissue particles. Serotonin release by connective tissue particles is probably not inhibited by FDP.

Effects of Halothane on Platelet Function

1980 ◽  
Vol 44 (03) ◽  
pp. 143-145 ◽  
Author(s):  
J Dalsgaard-Nielsen ◽  
J Gormsen
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Platelet Rich Plasma ◽  
Human Platelets ◽  
Halothane Anaesthesia ◽  
Inhibition Of Platelet Aggregation ◽  
Transient Impairment ◽  
High Concentrations ◽  
Uptake And Release ◽  
Platelet Functions

SummaryHuman platelets in platelet rich plasma (PRP) incubated at 37° C with 0.3–2% halothane for 5–10 min lost the ability to aggregate with ADP, epinephrine and collagen.At the same time uptake and release of 14C-serotonin was inhibited. When halothane supply was removed, platelet functions rapidly returned to normal. However, after high concentrations of halothane, the inhibition of platelet aggregation was irreversible or only partially reversible.The results suggest that halothane anaesthesia produces a transient impairment of platelet function.

Inhibition of Fibrinolytic Activity In-Vivo by Dexamethasone Is Counterbalanced by an Inhibition of Platelet Aggregation

1992 ◽  
Vol 68 (01) ◽  
pp. 069-073 ◽  
Author(s):  
J J J van Giezen ◽  
J W C M Jansen
Keyword(s):  
Platelet Aggregation ◽  
Fibrinolytic Activity ◽  
Ex Vivo ◽  
Dose Range ◽  
Coagulation System ◽  
Loop Model ◽  
Prothrombotic State ◽  
Inhibition Of Platelet Aggregation ◽  
Pai 1

SummaryDexamethasone decreases the fibrinolytic activity in cultured medium of several cell types by an induction of PAI-1 synthesis. As a result of this enhanced PAI-1 synthesis a prothrombotic state is expected in patients treated with dexamethasone. However, such a prothrombotic state is not reported as a major adverse effect. We have studied the effects of dexamethasone (dose range: 0.1–3.0 mg/kg) on the fibrinolytic system of rats after a 5 day pretreatment period. It appeared that dexamethasone dose dependently decreased the fibrinolytic activity (a dose of 1 mg/kg showed a reduction of about 40%). This reduced fibrinolytic activity could be functionally translated into an increased thrombus size as measured with a venous thrombosis model: thrombus size was increased by 50% with 1 mg/kg dexamethasone. No effects could be measured on the coagulation system, but it appeared that ex-vivo measured platelet aggregation was dose dependently inhibited by dexamethasone treatment. This effect resulted in-vivo in prolonged obstruction times as measured with a modified aorta-loop model. These results indicate that the expected prothrombotic state due to a diminished fibrinolytic activity caused by dexamethasone is counterbalanced by an inhibition of platelet aggregation.

Sign in / Sign up

Export Citation Format

Share Document