Reduction of Thrombus Formation on Dialyser Membranes by Aspirin and Ra 233

Lindsay, Robert M.; Ferguson, Denise; Prentice, C. R. M.; Burton, James; McNicol, G. P.

doi:10.1016/s0140-6736(72)92656-6

Cited by 83 publications

(29 citation statements)

References 13 publications

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“…In fact, the benefit in these patients has already been demonstrated [2,3,[5][6][7], Some workers have indicated apprehension in giving these drugs, feeling that bleeding may result from the abnormal platelet function [17,18]. The weight of evidence, however, indicates that these patients have increased in vivo [1][2][3][4][5][6][11][12][13] and in vitro [19] platelet activity, and this certainly enhances the atherogenic in dex.…”

Section: Discussionmentioning

confidence: 99%

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Enhanced in vitro Platelet Aggregation in Hemodialysis Patients

Viener¹,

Aviram²,

Better

et al. 1986

Nephron

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Hemodialysis patients suffer from premature atherosclerosis and various thrombotic and thromboembolic phenomena. Despite enhanced in vivo platelet activity, it is unclear whether in vitro platelet aggregation is increased or reduced in this population. We studied platelet aggregation in response to adenosine diphosphate and to epinephrine in 20 chronic hemodialysis patients and 21 controls. In the patient group the in vitro platelet aggregation was significantly enhanced in response to both aggregating agents. Our study demonstrated that in vitro platelet aggregation is enhanced in patients with chronic renal failure undergoing hemodialysis.

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Section: Discussionmentioning

confidence: 99%

“…This tendency appears to be less when administering drugs that depress platelet function [2,3,[5][6][7], These agents appear to deaccelerate [8] the development of premature atherosclerotic manifestations observed in these patients [9,10].…”

Section: Introductionmentioning

confidence: 99%

Enhanced in vitro Platelet Aggregation in Hemodialysis Patients

Viener¹,

Aviram²,

Better

et al. 1986

Nephron

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“…Platelet loss occurs by adhesion and aggregation onto the dialyser membrane, with associated fibrin deposition (Lindsay et al, 1972a), and by removal of platelets from the circulation within the patient (probably in the pulmonary vascular bed and spleen). Lindsay et al (1972b) have also reported that aspirin and dipyridamole protected the platelets and reduced dialyser blood loss. We have reported platelet sparing activity and reduced dialyser fibrin deposition with sulphinpyrazone (Woods et al, 1979), and more recently shown that prostacyclin can minimize platelet loss and reduce heparin requirement during regular haemodialysis (Turney et al, 1980).…”

Section: Introductionmentioning

confidence: 90%

Use of a thromboxane synthetase inhibitor, dazoxiben, during haemodialysis.

Dodd¹,

Gordge²,

Mj³

1983

Brit J Clinical Pharma

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1 We have assessed the thromboxane synthetase inhibitor, dazoxiben (UK 37248), during dialysis in a doubleblind, placebo-controlled crossover study. 2 Thromboxane generation was markedly inhibited, and there was an increase in serum 6-keto prostaglandin Fla levels during active treatment studies. 3 We were unable to demonstrate any reduction of platelet activation, or dialyser fibrin deposition, nor were heparin requirements altered by the drug. 4 Dazoxiben had no adverse effects.

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“…may serve as an in vivo fluid-phase indicator of platelet activation in clinical studies. An important role of cycloox ygenase-dependent steps in membrane/blood interaction is supported by clinical observa tions of reduced thrombus formation with aspirin [6] or indobufen [7], although the mechanisms involved may be more complex because aspirin has also been shown to alter protein membrane interaction [8].…”

Section: Mechanisms Of Activation Of Hemostatic Systemsmentioning

confidence: 99%

Dialysis Membranes and Coagulation System

et al. 1986

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Artificial membranes used for hemodialysis differ from endogenous membranes, i.e. endothelial cells, by their variable thrombogenicity. The key step in activation of the coagulation system by dialysis membranes is thrombocyte activation which is preceded by formation of a protein layer of critical thickness. Crucial questions concerning the quality of this protein membrane as a determinant of thrombocyte activation are not well understood. Activation of the contact phase of the intrinsic plasmatic coagulation system by dialysis membranes is well documented. Local action of thrombin in the membrane microenvironment is documented by release of fibrinopeptide A and deposition of fibrin on the membrane. Apart from thrombin, other mechanisms, e.g. PMN elastase, plasma-independent activation of blood cells, facilitatory action of erythrocytes etc., may play a contributory role. With respect to the polycarbonate membrane, some authors find less platelet extraction and unchanged platelet release reaction. In our own studies, polycarbonate membranes were not superior to cuprophane membranes with respect to thrombogenicity.

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Reduction of Thrombus Formation on Dialyser Membranes by Aspirin and Ra 233

Cited by 83 publications

References 13 publications

Enhanced in vitro Platelet Aggregation in Hemodialysis Patients

Enhanced in vitro Platelet Aggregation in Hemodialysis Patients

Use of a thromboxane synthetase inhibitor, dazoxiben, during haemodialysis.

Dialysis Membranes and Coagulation System

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