The Mechanism of Platelet Aggregation in Relation to Hemostasis

Käser-Glanzmann, R.; Lüscher, E. F.

doi:10.1055/s-0038-1655397

Cited by 47 publications

(10 citation statements)

References 13 publications

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“…Since the larger spheroids are free of granules and contain little ground substance, they probably represent the inactive part of the platelet. The failure of formation of pseudopodia in vitro is in accordance with the in vivo findings in which platelets con tacted HIPA tumor cells without formation of pseudopodia [10], Inhibition of pseudopodia formation in vitro is probably a rather nonspecific phenomenon and may be due to different exogenous plate let-damaging agents, as platelet agglutinins or other factors [5,11]. In other cases, it may be caused by an inherent defect in platelets, as in thromboasthenia [1].…”

Section: Discussionsupporting

confidence: 76%

Interaction of Platelets with Ascitic Plasmacytoma <i>in vitro</i>

Pedio¹,

Rüttner²,

Odermatt³

1973

Acta Haematol

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During interaction in vitro of syngenic platelets from healthy mice with HIPA ascitic plasmacytoma, clot formation was slower than during interaction of syngenic platelets from HIPA tumor-bearing mice with HIPA plasmacytoma. The platelet aggregates were composed, in both cases, of ‘balloon platelets’ and tumor cells. The granulated part of the ‘balloon platelets’ made up the centre, whereas granule-free spheroids were seen at the periphery of the aggregates. To contact with platelets, the tumor cells reacted with formation of microvilli, condensation of mitochondria and phagocytosis of the granule-free spheroids. No formation of pseudopodia by platelets in contact with the tumor cells was observed.

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Section: Discussionsupporting

confidence: 76%

Interaction of Platelets with Ascitic Plasmacytoma <i>in vitro</i>

Pedio¹,

Rüttner²,

Odermatt³

1973

Acta Haematol

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“…It has been suggested that thrombin-induced aggregation of platelets is mediated through ADP (34). Plasmin-treated platelets contained almost normal amounts of ATP, which was released by addition of thrombin, yet these platelets did not aggregate.…”

Section: Resultsmentioning

confidence: 99%

Role of Platelet Fibrinogen in the Reactions of Platelets to Thrombin*

Morse¹,

Jackson²,

Conley³

1965

J. Clin. Invest.

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Washed human blood platelets contain a clottable protein that is similar to, if not identical with, plasma fibrinogen (1-4). After incubation with trypsin under appropriate conditions, platelets remain morphologically intact but no longer contain clottable protein (5). Trypsinized platelets, unlike normal platelets, are not aggregated by fresh serum or by a solution of thrombin and calcium chloride. When resuspended in plateletfree plasma or in a buffered solution of fibrinogen containing glucose, trypsinized platelets produce retraction of clots formed by thrombin; during the formation of the clot and its subsequent retraction, trypsinized platelets aggregate and undergo the usual changes of viscous metamorphosis (5). These observations suggest that fibrinogen on the surface of platelets is involved in the reaction of platelets to thrombin. This reaction does not consist simply of the coagulation of fibrinogen with entrapment of platelets in the fibrin mesh. Under usual conditions divalent cations are required for thrombin-induced platelet aggregation but not for clotting of fibrinogen (5, 6). Electron photomicrographs of platelet aggregates show no striated fibrin strands between adherent

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“…The continued production of thrombin and adenosine diphosphate, however, is insured by par,ticipation of platelets. Kaser-Glanzmann and Luscher (1962) 29 have shown that platelets contain enough adenosine triphosphate, which on degradation could account for all the platelet aggregation. By 30 seconds extensive platelet aggregation has taken place and sufficient platelet disintegration within aggregates may then account for released platelet factor 3 to activate plasma prothrombin to thrombin.…”

Section: B Formation Of Hemostatic Plugsmentioning

confidence: 99%

The Function of Platelets

et al. 1966

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The main function of platelets, the maintenance of hemostasis, depends on three of their properties, the endothelial supporting function of platelets, the ability to form hemostatic plugs and to release lipoprotein material (platelet factor 3). When the number of circulating platelets is reduced the capillary endothelium becomes weakened as platelets are not available to enter the endothelial cytoplasm to support it and the capillary wall ruptures when exposed to minor trauma. The bleeding through the ruptured vessel wall is arrested by formation of a clump of platelets forming a hemostatic plug. Damage to the vessel wall initiates both the coagulation mechanisms and degradation of adenosine triphosphate. The products of each of these reactions, namely, thrombin and adenosine diphosphate bring about aggregation of platelets to form the hemostatic plug. These are the platelet functions performed following a transfusion of platelets into a thrombocytopenic recipient. The platelets remaining in the circulation and which are counted in platelet survival studies are those in excess of the immediate need of the recipient.

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The Mechanism of Platelet Aggregation in Relation to Hemostasis

Cited by 47 publications

References 13 publications

Interaction of Platelets with Ascitic Plasmacytoma <i>in vitro</i>

Interaction of Platelets with Ascitic Plasmacytoma <i>in vitro</i>

Role of Platelet Fibrinogen in the Reactions of Platelets to Thrombin*

The Function of Platelets

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