Haemostasis in the Microvasculature of the Rabbit Mesentery, Effects of some Pharmacological Agents of Current Interest in Haemostasis and Thrombosis

Bergqvist, David; Arfors, Karl-E.

doi:10.1159/000214121

Cited by 4 publications

(2 citation statements)

References 17 publications

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“…In an earlier study the administration of reserpine which induces depletion of platelet contents had no effect on PHT or THT (16). The serotonin mediated vessels contraction seems thus to be of little importance in initial microvessel hemostasis.…”

Section: Discussionmentioning

confidence: 81%

The Effect of Serotonin Inhibition on Initial Microvessel Hemostasis and Platelet Aggregation In Vivo

et al. 1983

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SummaryThe role of serotonin (5-HT) in initial microvascular hemostasis is not fully understood. This study was made to evaluate the effect on hemostatic plug formation and laser-induced arteriolar microembolism of different substances which counteract the effect of 5-HT. Hemostatic plug formation time and stability was measured in the rabbit mesenteric microcirculation and laserinduced embolism in the rabbit ear chamber. Ketanserine, a selective 5-HT2-receptor blocker shortened arteriolar hemostatic plug formation time. Dihydroergotamine, an unselective blocker (with 5-HT- and α-adrenergic receptor affinity) increased venular hemostatic plug formation time and also decreased the hemostatic plug stability. Laser-induced platelet embolism was unaltered after both ketanserine and dihydroergotamine administration. The magnitude of these changes seems to exclude an important effect of 5-HT in initial microvessel hemostasis or on platelet activity.

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Section: Discussionmentioning

confidence: 81%

The Effect of Serotonin Inhibition on Initial Microvessel Hemostasis and Platelet Aggregation In Vivo

et al. 1983

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“…Animal models of venous thrombosis have been widely used in the evaluation of the antithrombotic actions of heparin and related substances. 1,3,5,6,[9][10][11][12]19 since its introduction, the Wessler stasis thrombosis model has been widely used for the evaluation of the antithrombotic action of drugs and the thrombogenic action of numerous agents. 2,4,7,8,21,22,25 Although this model has provided useful information on the nature of the antithrombotic actions of heparin and derivatives, the results obtained are relative to the type of thrombogenic agent used, 12,13,20 that is, the observed antithrombotic actions of a drug depend on the type of challenge used to produce the thrombotic processes.…”

mentioning

confidence: 99%

A Modified Stasis Thrombosis Model to Study the Antithrombotic Actions of Heparin and Its Fractions

Fareed¹,

Walenga²,

Kumar³

et al. 1985

Semin Thromb Hemost

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The original stasis thrombosis model of Wessler has been modified. Numerous thrombogenic agents were evaluated for their pathophysiologic effects and were classified in terms of stasis clot in the jugular vein. Alterations produced in coagulation parameters, such as the PT, APTT, thrombin time, activated recalcification time (Hemachron), and thrombelastographic pattern were recorded. Since the pathophysiologic activation of the hemostatic system varies considerably in different diseases, a proper animal model along with a proper type of thrombogenic trigger should be carefully selected to produce pathogenesis and to study the therapeutic responses of heparin and its derivatives. In the modified stasis thrombosis model, besides monitoring the formation of the jugular vein stasis clot, it is proposed that the following tests may be useful to establish hypercoagulable states: Functional levels of various coagulation factors, platelet counts, fibrinogen levels, and whole blood activated clotting times. The nature of activation processes in each thrombogenic challenge should be carefully analyzed in terms of pathways involved; for example, the administration of heterologous serum (such as human, monkey) to rabbits produces anaphylactoid reactions, including hemolysis, thrombocytopenia, clinical chemistry abnormalities (enzymes), and many problems that may involve the complement and immune systems. All previous data obtained using heterologous sera as a thrombogenic trigger are of questionable value as to the efficacy of some of the antithrombotic agents tested against it. In addition to the species and the thrombogenic challenge, the following factors may contribute significantly to the pathophysiologic response and its alteration by various agents: (1) Composition of the thrombogenic agent; (2) effect of preparatory drugs, such as anesthetics, on the hemostatic parameters; (3) alterations on injection time, volume, osmolarity, and temperature; (4) variations in the circulation time of the thrombogenic agent and stasis time of the ligated jugular vein stasis segment; and (5) blood sample collection and handling. Since the kallikrein-kinin cascade is closely associated with the coagulation and the fibrinolytic network, a systemic monitoring of blood pressure may provide information on the effect of thrombogenic agents on hemodynamics.(ABSTRACT TRUNCATED AT 400 WORDS)

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Influence of dextrans on platelet distribution in arterioles and venules

et al. 1993

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Dextrans bind to the surface of platelets, red blood cells and endothelium. We investigated whether a low doses (30 mg/kg IV) of 40-kDa (Dx40), neutral, 500-kDa (Dx500) or sulphated, 500-kDa (Dx500S) dextrans influence platelet distribution in rabbit mesenteric arterioles and venules (diameter 17-33 microns). Intravital fluorescence videomicroscopy was used to visualize platelets labelled in vivo with acridine red. Their concentration distribution determined within a thin optical section about the median vessel plane was expressed relative to the mean concentration in that vessel. In arterioles, Dx500 and Dx500S increased the relative platelet concentration in the centre [radial position (R): 0.0-0.4 R] from 0.60 to 1.07 (P < 0.001) and 1.20 (P < 0.003), and reduced it near the wall (0.8-0.9 R) from 1.59 to 0.93 (P < 0.02) and 0.95 (P < 0.03) respectively. In venules a similar, but non-significant, effect was observed. Dx40 did not change platelet distribution in arterioles, but decreased their concentration in venules in the centre from 1.08 to 0.71 (P < 0.03) and increased it at the wall from 0.89 to 1.27 (P < 0.04). The deformability of red blood cells was unchanged, but their aggregation tendency increased approximately two-fold after Dx500 and Dx500S injection, while Dx40 had no influence. Leucocyte margination in venules did not affect platelet distribution. Dextran injection did not change microvascular flow velocity or plasma viscosity, suggesting that the observed changes in arteriolar platelet distribution were caused by binding of dextran to the surface of platelets and/or red blood cells.

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Haemostasis in the Microvasculature of the Rabbit Mesentery, Effects of some Pharmacological Agents of Current Interest in Haemostasis and Thrombosis

Cited by 4 publications

References 17 publications

The Effect of Serotonin Inhibition on Initial Microvessel Hemostasis and Platelet Aggregation In Vivo

The Effect of Serotonin Inhibition on Initial Microvessel Hemostasis and Platelet Aggregation In Vivo

A Modified Stasis Thrombosis Model to Study the Antithrombotic Actions of Heparin and Its Fractions

Influence of dextrans on platelet distribution in arterioles and venules

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