Aprotinin effect on platelet function and clotting during cardiopulmonary bypass

Tabuchi, Noriyuki; Dehaan, J; Boonstra, PW; Huet, Rcgg; Vanoeveren, W

doi:10.1016/1010-7940(94)90098-1

Cited by 27 publications

(5 citation statements)

References 10 publications

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“…Tabuchi et al, however, further distinguished the effect of a plasmin-inhibiting dose of aprotinin on platelet glycoprotein expression. 32 Although the plasmin-inhibiting dose of aprotinin preserved platelet adhesive function during CPB via improved GpIb antigen expression during CPB as compared with controls, platelet GpIIb/IIIa antigen and ADP aggregation were not different between the aprotinin and control groups. In total, these results suggest that any improved platelet function observed with the plasmin-inhibiting dose of aprotinin in CPB surgery may be attributable, in part, to the preserved adhesive capacity and function of the GpIb platelet receptor.…”

Section: Plateletsmentioning

confidence: 86%

“…Effects on PAR1 may help to explain why the GpIb receptor activity appears to be preserved with the plasmin-inhibiting-dose of aprotinin, whereas platelet preservation effects are not typically observed with lysine analogs. [30][31][32] In addition, lower plasmininhibiting doses of aprotinin will likely have reduced effects to inhibit the generation of thrombin, a kallikrein-dependent effect. [24][25][26][27][28] Thus, in contrast to speculation that aprotinin may be prothrombotic, data clearly indicate that aprotinin has significant antithrombotic properties.…”

Section: Plateletsmentioning

confidence: 99%

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Antiinflammatory Effects of Aprotinin

Taylor

2004

Transfus Alt Transfus Med

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SUMMARY Aprotinin is a serine protease inhibitor that binds to human serine proteases with various affinities. This small protein has profound effects on the systemic inflammatory response syndrome induced by cardiopulmonary bypass. The intersecting pathways of complement, cytokines, coagulation, fibrinolytic, and kinin‐kallikrein systems all converge with tremendous amplification and potentially damaging effects to the patient. Aprotinin exerts a dose‐dependent inhibition of plasmin and kallikrein activities. Activation of these entities occurs ‘early’ in their respective pathways, and inhibition by aprotinin has downstream implications such as reducing the generation of thrombin, to minimize amplification of systems involved in the systemic inflammatory response. More localized effects of aprotinin at the level of the neutrophil, endothelial cell interaction or platelet‐thrombin interaction can have significant effects in terms of minimizing the damage to organs and tissues. The antiinflammatory effects associated with aprotinin treatment, in tandem with the hemostatic action, result in beneficial outcomes for many patients.

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Section: Plateletsmentioning

confidence: 86%

Section: Plateletsmentioning

confidence: 99%

Antiinflammatory Effects of Aprotinin

Taylor

2004

Transfus Alt Transfus Med

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“…However, aprotinin did not have an additional effect on the platelet release reaction, as demonstrated by the similar levels of the α‐granule component, P‐selectin. These findings suggest an effect of aprotinin on platelet adhesive or aggregatory receptors in agreement with the findings of others ( Bidstrup et al , 1989 ; Mohr et al , 1992 ; Tabuchi et al , 1994 ). The mechanism of action remains unclear, but may indicate a direct effect on platelets ( Najman et al , 1993 ).…”

Section: Discussionmentioning

confidence: 99%

Aprotinin complements heparin bonding in an in vitro model of cardiopulmonary bypass

Bannan

Martín

1998

Br J Haematol

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Summary.The relative contribution of full-dose aprotinin, used with heparin-bonded surfaces, to contact activation during cardiopulmonary bypass was examined. In vitro Carmeda-bonded cardiopulmonary bypass circuits were perfused with whole blood anticoagulated with heparin (3·3 U/ml). Aprotinin (300 kIU/ml) was added to the circuits of one set of experiments. Samples were taken prior to perfusion and at 30, 60, 120 and 360 min. The activated coagulation time was extended in the aprotinin experiments, significantly at 30 min (P ¼ 0·003) and 120 min (P ¼ 0·001). Thrombin-antithrombin complexes and prothrombin fragment F1þ2 were both higher in the nonaprotinin experiments at 120 min (P ¼ 0·02 each) and 360 min (P ¼ 0·005 and 0·001, respectively). Plasma leucocyte elastase was raised in the non-aprotinin experiments in comparison to the aprotinin experiments at each timepoint (30 min, P ¼ 0·04; 60 min, P ¼ 0·006; 120 min, P ¼ 0·001; 360 min, P ¼ 0·0001), as was interleukin-8 at 120 min (P ¼ 0·05) and 360 min (P ¼ 0·0001). No differences were found for the platelet activation marker P-selectin. Platelet and white blood cell counts fell significantly in the non-aprotinin experiments compared with the aprotinin experiments at 360 min (P ¼ 0·05 and 0·03, respectively). It would appear that the use of aprotinin has additional haemostatic beneficial effects to those found with heparin-bonded circuits in terms of effects on contact activation and inflammation.

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“…4 A decreased expression of GPIb has therefore been suggested to lead to a decreased adhesive capacity and thus to result in prolonged bleeding and excessive blood loss. 2,5 This hypothesis has been confirmed by the finding that administration of aprotinin, a bovine protein that acts as a nonselective inhibitor of serine proteases, prevented the disappearance of GPIb and simultaneously reduced the blood loss and the use of blood products during CPB. 6 Several investigators could not demonstrate the disappearance of GPIb, however, and decreased expression of GPIb in systemic blood therefore remains under debate.…”

mentioning

confidence: 89%