Inhibition of platelet-vessel wall interactions by thromboxane receptor antagonism in a human in vitro
 system: potentiation of antiplatelet effects of aspirin

SummaryAn in vitro system is described in which adhesion of blood platelets to washed and tannic acid-treated red cells was assayed quantitatively by microscopic observation. ADP, epinephrine and TAME produced a reversible increase in platelet adhesiveness which was antagonized by AMP. With Evans blue, polyanetholsulfonate, phthalanilide NSC 38280, thrombin and heparin at concentrations above 1-4 u/ml the increase was irreversible. The ADP-induced increase in adhesiveness was inhibited by sodium citrate, EDTA, AMP, ATP and N-ethylmaleimide. EDTA, AMP and the SH-blocker N-ethylmaleimide also reduced spontaneous platelet adhesion to red cells. No significant effects were observed with adenosine, phenprocoumon, 5-HT, phthalanilide NSC 57155, various estrogens, progestogens and fatty acids, acetylsalicylic acid and similarly acting agents, hydroxylamine, glucose and KCN. The method may be useful for the screening of thrombogenic and antithrombotic properties of drugs.

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The Mesothelial Cell as a Non-Thrombogenic Surface

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661149 ◽

1984 ◽

Vol 52 (02) ◽

pp. 102-104 ◽

Cited By ~ 25

Author(s):

L J Nicholson ◽

J M F Clarke ◽

R M Pittilo ◽

S J Machin ◽

N Woolf

Keyword(s):

Electron Microscopy ◽

Scanning Electron Microscopy ◽

Blood Flow ◽

Cell Surface ◽

Mesothelial Cell ◽

Mesothelial Cells ◽

Plastic Film ◽

In Vitro System ◽

Scanning Electron

SummaryA technique for harvesting mesothelial cells is described. This entails collagenase digestion of omentum after which the cells can be cultured. The technique has been developed using the rat, but has also been successfully applied to human tissue. Cultured rat mesothelial cells obtained in this way have been examined by scanning electron microscopy. Rat mesothelial cells grown on plastic film have been exposed to blood in an in vitro system using a Baumgartner chamber and have been demonstrated to support blood flow. No adhering platelets were observed on the mesothelial cell surface. Fibroblasts similarily exposed to blood as a control were washed off the plastic.

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Establishing an in vitro system to study chondrocyte phenotypes associated to human hereditary hemochromatosis and identify molecular players involved in chondrocyte related iron metabolism

Bone Abstracts ◽

10.1530/boneabs.1.pp262 ◽

2013 ◽

Author(s):

Marcio Simao ◽

Paulo Gavaia ◽

Jorge Pinto ◽

Ea Korng ◽

M Leonor Cancela

Keyword(s):

Iron Metabolism ◽

Hereditary Hemochromatosis ◽

In Vitro System

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Faculty Opinions recommendation of Coupling of human DNA excision repair and the DNA damage checkpoint in a defined in vitro system.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718232039.793490409 ◽

2014 ◽

Author(s):

Paul Nghiem ◽

Kaifeng Hung

Keyword(s):

Dna Damage ◽

Excision Repair ◽

Dna Damage Checkpoint ◽

In Vitro System ◽

Dna Excision Repair ◽

Human Dna

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Thrombogenicity of the Injured Vessel Wall – Role of Antithrombin and Heparin

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642399 ◽

1994 ◽

Vol 71 (01) ◽

pp. 147-153 ◽

Cited By ~ 22

Author(s):

Siw Frebelius ◽

Ulf Hedin ◽

Jesper Swedenborg

Keyword(s):

Vessel Wall ◽

Antithrombin Iii ◽

Rabbit Aorta ◽

Continuous Treatment ◽

Balloon Injury ◽

Coagulant Activity ◽

Risk For Thrombosis ◽

Inhibition Of Thrombin

SummaryThe thrombogenicity of the vessel wall after endothelial denudation is partly explained by an impaired inhibition of thrombin on the subendothelium. We have previously reported that thrombin coagulant activity can be detected on the vessel wall after balloon injury in vivo. The glycosaminoglycans of the subendothelium differ from those of the endothelium and have a lower catalyzing effect on antithrombin III, but inhibition of thrombin can still be augmented by addition of antithrombin III to the injured vessel surface.In this study the effect of antithrombin III and heparin on thrombin coagulant activity on the vessel wall was studied after in vivo balloon injury of the rabbit aorta using biochemical and immunohistochemical methods and thrombin was analysed after excision of the vessel. Continuous treatment with heparin, lasting until sacrifice of the animal, or treatment with antithrombin III resulted in significant reduction of thrombin coagulant activity on the injured aorta. Heparin given only in conjunction with the injury did not prevent thrombin coagulant activity or deposition of fibrin on the surface.The capacity of the injured vessel wall to inhibit thrombin in vitro was improved on aortic segments obtained from animals receiving antithrombin III but not from those given heparin. It is concluded that treatment with antithrombin III interferes with thrombin appearance on the vessel wall after injury and thereby reduces the risk for thrombosis.

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