Relase of retraction stimulating factor (RSF) during platelet dependent retraction of reptilase clots.
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Batroxobin↗
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Platelet shape change induced by cold and the retraction of reptilase clots.
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Batroxobin↗
Acquired IgG antibody occurring in a thrombasthenic patient: its effect on human platelet function.
In subagglutinating amounts, an IgG antibody isolated from the plasma of a polytransfused thrombasthenic patient (L) inhibited ADP-, epinephrine-, collagen-, and thrombin-induced aggregation of normal human platelets. The inhibition of ADP-induced aggregation was strongly diminished following the prior incubation of the antibody with control human platelet stroma but not with the stroma prepared from the platelets of two different thrombasthenic patients. The IgG(L) did not affect the binding of 14C-ADP to control human platelet membranes and did not inhibit the ADP-induced shape change. Bovine factor VIIIVWF-induced agglutination and ristocetin-induced aggregation of control human platelets were not inhibited in the presence of the antibody. The IgG(L) strongly inhibited ADP-induced retraction of reptilase clot and thrombin-induced clot retraction. This antibody therefore induced a thrombasthenialike state in normal human platelets, suggesting that the antigenic site recognized by the antibody plays a central role in the later stages of the mechanism of platelet aggregation induced by physiologic aggregation-inducing agents.
Adenosine Diphosphate↗
Tanshinone IIA impairs platelet function and thrombus formation.
BACKGROUND: Tanshinone IIA (T-IIA) is a fat-soluble active ingredient derived from the traditional Chinese medicine Danshen and possesses cardioprotective property. However, its exact role in platelet function is unknown. OBJECTIVES: This study investigated T-IIA's role in platelet aggregation, granules release, spreading, clot retraction, as well as in vivo hemostasis and thrombus formation. METHODS: Human platelets were treated with different doses of T-IIA (10, 50, and 100 μM) to measure platelet function and activation. In addition, T-IIA was administrated into wild-type mice to evaluate hemostasis and thrombus formation. RESULTS: T-IIA significantly impaired platelet aggregation, adenosine triphosphate secretion, P-selectin expression, and spreading and clot retraction dose dependently without affecting the expression profiles of αIIbβ3 and glycoprotein VI or Ibα. Administration of T-IIA significantly prolonged mice tail bleeding time and inhibited arterial and venous thrombosis. Further analysis showed that T-IIA dose dependently reduced platelet reactive oxygen species generation. Quantitative proteomic and phosphoproteimic assays analyzing T-IIA-treated vs vehicle-treated platelets after stimulation identified dysregulated phosphorylation of several proteins, which were enriched in platelet activation. Among the downregulated phosphoproteins, Rho-associated protein kinase (ROCK)1, integrin β3, and talin1 exhibited the lower fold change of phosphorylation in T-IIA-treated platelets compared with those in vehicle-treated platelets. Consistently, T-IIA treatment inhibited the phosphorylation of ROCK1, p47phox, integrin β3, and talin1 in activated platelets. CONCLUSION: T-IIA impairs platelet function and thrombosis via inhibition of several signaling pathways including ROCK1/p47phox, β3, and talin1, implying that T-IIA may represent a promising therapeutic candidate for treating thrombotic diseases.
Animals↗
Platelets and platelet function in patients with chronic uremia on maintenance hemodialysis.
In 20 chronic uremic patients on maintenance hemodialysis, who were not taking any medication known to affect platelet function, the following investigations were carried out: platelet count, fibrin/fibrinogen degradation products, fibrinogen and plasminogen concentration, platelet adhesiveness, clot retraction and platelet aggregation induced by ADP, ristocetin, fibrinogen, collagen and epinephrine. The only significant abnormal result was a decreased clot retraction. We consider many cases of so-called uremic bleeding to be caused by the medication taken and conclude that on well-controlled hemodialysis treatment, bleeding tendency should not be a major problem.
Blood Coagulation Disorders↗
Plateletpheresis by discontinuous centrifugation: effect of collecting methods on the in vitro function of platelets.
The in vitro function of platelets collected by two different methods during centrifugal plateletpheresis was compared. The RBC method involves collecting platelets with red cells followed by a supplementary spin to remove them, whereas the no-RBC method requires collecting platelets only from the buffy coat without red cells. Platelet response to adenosine diphosphate (ADP), epinephrine and collagen was slightly reduced in platelet-rich plasma (PRP) prepared by no-RBC technique and was markedly decreased in samples obtained by the RBC technique when compared to prepheresis controls. The decrease in platelet response to ADP, epinephrine and collagen was apparent in three testing systems: aggregation, release of serotonin and reptilase clot retraction. Both plasma and platelets appeared to be affected by the pheresis procedure. Platelet preparations obtained by both RBC and no-RBC techniques showed an increase of platelet factor 3 activity and an enhancement of aggregation, release of serotonin and clot retraction induced by thrombin as compared to prepheresis controls. Postpheresis platelet-poor plasma contains platelet membrane fragments which exhibit a high platelet factor 3 activity. The results showed that the RBC method, although providing a higher platelet yield, caused more qualitative alterations in platelets than in those obtained by no-RBC method, and that both methods of collecting platelets activated the procoagulant activity of platelets.
Blood Platelets↗
Binding of anti-actin autoantibodies to platelets.
Normal platelets incubated with anti-actin autoantibodies (AAA) (from the serum of patients with chronic aggressive hepatitis) do not show binding of these antibodies as seen by indirect immunofluorescence. AAA serum does not inhibit thrombin-induced clot retraction, despite the binding of the antibodies to platelets in the clot. Similarly, AAA serum does not affect "reversible" or "irreversible" aggregation (induced by ADP, collagen or epinephrine), despite the binding of the antibodies to platelet actin under such circumstances. AAA also bind to platelets when aggregation is inhibited by EDTA. The incubation of "reversibly" aggregated platelet with AAA results in a small but definite binding of AAA to platelets. These findings suggest that during "irreversible" and/or "reversible" aggregation, changes take place at the surface of platelets which expose the antigen at the surface of the cell.
Actins↗
Necrosis, haemorrhage and complement depletion following bites by the spitting cobra (Naja nigricollis).
The Spitting Cobra, Naja nigricollis, is widely and densely distributed in Africa. Fourteen patients with proven N. nigricollis bites, who were seen in the savanna region of Nigeria, did not exhibit the neurological signs, such as cranial nerve lesions and respiratory paralysis, expected following Elapid poisoning. All had local swelling, in eight cases involving the entire limb, and ten developed local tissue necrosis. Spontaneous haemorrhage was detected in three cases and was the probable cause of death in one of them; the other death in this series was unexplained. Haematological abnormalities included prolonged clot lysis anf failure of clot retraction due to a platelet defect. There was no specific deficit in clotting factors and a delayed rise in fibrin degradation products was attributed to extensive tissue damage at the site of the bit. Most patients showed depletion of complement component C3 and glycine-rich beta-glycoprotein (GBG), suggesting activation of the alternative pathway of complement fixation. There was evidence of hepatocellular damage in two out of six patients investigated. There was no evidence that specific polyvalent antivenoms, used in doses of up to 80 ml, prevented any of the effects of N. nigricollis venom. Clinical laboratory diagnosis is discussed. In the past many bites were wrongly classified as viper bites on the basis of clinical findings. Immunodiagnosis is a promising method for assessing the true importance of N. nigricollis bite in West Africa.
Adolescent↗
Analysis and interpretation of the impedance blood coagulation curve.
The impedance coagulation curve represents the relationship between the changing impedance of a clotting blood sample and the impedance of a heparinized control sample. The impedance method is independent of the conventional technics for coagulation studies and offers, therefore, new perspective into the study of the coagulation process. The technic provides accurate measures of the whole-blood clotting time and clot retraction time and has higher diagnostic power than current methods for whole-blood clotting time determination. The purpose of this study was to reveal the mechanism of the impedance changes and to explore the curve for additional information relevant to clinical or theoretical problems. It is established that before clotting the curve reflects "lag" and "activation" phases that strongly suggest a "cascade mechanism" of coagulation activation. The mechanisms of other parts of the curve are explained and their possible relevances to the coagulation process are discussed.
Blood Coagulation↗
Ditazole and platelets. I. Effect of ditazole on human platelet function in vitro.
Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) has been shown to be a strong in vitro inhibitor of human platelet aggregation brought about by release reaction inducers; in contrast, it did not significantly affect primary ADP-induced aggregation. Ditazole strongly inhibited the release of platelet-bound 14C-serotonin under the influence of Thrombofax, whereas it did not interfere with the transport and storage of serotonin in nonstimulated platelets. The effect of ditazole was not potentiated by acetylsalicylic acid. Ditazole also inhibited ADP-reptilase clot retraction and modified thrombin-induced clot formation. The inhibition of platelet aggregation exerted by ditazole in plasma could be removed following gel filtration of platelets on Sepharose 2-B gel. This would indicate that ditazole does not act on platelets by a 'hit and run' mechanism.
Adenosine Diphosphate↗
Effect of vitamin E on platelet aggregation in diabetic retinopathy.
The effect of vitamin E on platelet aggregation was investigated in a group of 10 patients with diabetic retinopathy. Adenosine diphosphate induced platelet aggregation was inhibited in the patients' group as well as in the controls in the presence of vitamin E. An increased platelet aggregation was obtained with arachidonic acid in both groups when platelet-rich plasma was incubated prior with vitamin E. The clot retraction inhibition test parallels the findings of aggregation obtained with the platelet aggregation meter.
Adenosine Diphosphate↗
Biochemical mechanism of platelet activation. Involvement of contractile proteins.
The present state of knowledge of the biochemical mechanism of platelet activation (adhesion, shape change, microspike formation, aggregation, release reaction, clot retraction) is presented under involvement of contractile proteins. The working hypothesis on the contractile mechanism of platelet activation is explained.
Actomyosin↗
Platelet hyperaggregability and thrombosis in patients with thrombocythemia.
The relation between platelet hyperaggregability and thrombosis was assessed in 28 patients with thrombocythemia due to myeloproliferative diseases and 11 with reactive thrombocytosis. None of the patients with reactive thrombocytosis had thrombotic or hemorrhagic complications, but thrombosis was noted in seven patients and bleeding in two patients with thrombocythemia. Nineteen were asymptomatic. In patients with thrombosis, bleeding time, platelet glass retention, and clot retraction were normal, but evidence of platelet hyperaggregability was present in all but one. Serial studies on six patients revealed a close association between platelet hyperaggregability and ischemic attacks. Neither patient with bleeding complications had evidence of platelet hyperaggregability, although poor platelet function was found in one. Platelet function in asymptomatic patients can be classified as hyperactive, hypoactive, or normal.
Adult↗
[Effect of phosphatidylserine on formation and lysis of fibrin].
Phosphatidyl serine inhibited non-enzymatic step of fibrin formation (selfassociation of monomeric fibrin). But phosphatidyl serine did not affect the factor XIII activity, the rate of fibrin clot retraction and its tolerance to plasmin. Activity of plasmin was not altered in presence of phosphatidyl serine but influence of slowly acting antiplasmin on plasmin was slightly limited by the lipoid. Due to this phenomenon phosphatidyl serine caused the activation of fibrinolysis in native system (blood plasma). The data obtained support the earlier advanced assumptions on inhibition of thrombin-fibrinogene reaction by phosphatidyl serine.
Antifibrinolytic Agents↗
Inhibition of collagen-induced platelet aggregation by antibodies to distinct types of collagens.
Aggregation of platelets by fibrils formed from collagens type I, II and III could be inhibited by coating the fibrils with anti-collagen antibodies or Fab fragments. Similar results were obtained in a clot-retraction assay. Inhibition was achieved with stoichiometric amounts of antibodies and was specific for each type of collagen. Aggregation caused by a mixture of type-I and -III collagens could only be inhibited by a mixture of antibodies against both collagens. The data show that each interstitial collagen is capable of interacting with platelets and do not support the concept of an outstanding activity of type-III collagen.
Antibodies↗
Specificity of the effects of cytochalasin B on transport and motile processes.
The effects of cytochalasin B (CB) and dihydrocytochalasin B (H2CB) on a variety of transport and motile processes have been compared. CB inhibited transport of D-glucose and L-glucose but not transport of thymidine in human erythrocytes. In contrast, H2CB, which differs from CB by the absence of a single double bond, had little or no effect on any of these processes. Both cytochalasins, however, affected the morphology of cultured fibroblasts and inhibited motile processes such as membrane ruffling, axon growth cone activity, blood clot retraction, cytoplasmic streaming, photodinesis, and cytokinesis. Determination of the partition coefficient of the two cytochalasins in several organic solvent/phosphate-buffered saline systems showed that H2CB has a higher affinity for the hydrophobic phase than CB. These results indicate that the inhibitory effects of CB on sugar transport and on cell motility and morphology are separable and independent events, mediated by the binding of the drug to specific cellular receptors.
Axons↗
[Microcirculation and blood coagulation in patients with diabetes mellitus undergoing antidiabetic therapy of different types].
A comparative study of the peculiarities of the course of diabetes and metabolic disturbances, and also of the indices of capillary permeability, biomicroscopy of the conjunctival vessels, platelet aggregation, coagulorgam and blood clot retraction was carried out in the group of patients treated with insulin and sacharreducing sulfanilamides. Marked derangements in the microcirculatory system concerning both the vascular wall proper and of the rheological properties of the blood were revealed. These derangements were more distinct in the patients over 45 years of age with prolonged affection and the presence of vascular complications but proved to be independent of the therapy carried out.
Adult↗
Conjunctival bleeding in Osler's disease with associated platelet dysfunction. A case report.
A patient with Osler's disease (hereditary haemorrhagic telangiectasia) was admitted to hospital because of obstinate, profuse conjuctival bleeding occurring without any known preceding rrauma. Extensive examination of the haemostatic mechanism revealed an impaired platelet function reflected in defective platelet aggregation by ADP, collagen adrenalin and defective clot retraction. This platelet dysfunction, whose association with conjunctival telangiectasia was hitherto unknown, impaired the patient's already deficient primary haemostasis following the vascular anomaly and apparently contributed to the severity of the bleeding which could only be checked surgically. The findings seem to warrant investigation of the platelet function in patients with Osler's disease. In the event of platelet dysfunction drugs, such as acetylsalicylic acid (aspirin), indomethacin, dextrans as well as transfusions with bank blood are contraindicated.
Adenosine Diphosphate↗