Loss of platelet fibrinogen receptors during clinical cardiopulmonary bypass

Rk, Wenger; Łukasiewicz, H; Bs, Mikuta; Niewiarowski, Stefan; Edmunds, L. Henry

doi:10.1016/s0022-5223(19)35329-2

Cited by 150 publications

(41 citation statements)

References 18 publications

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“…On the other hand, avoidance of haemorrhage is important, because haemostasis is vital during and after ECMO [10] and CPB [2,11]. There is evidence that thrombocytopenia due to consumption of activated platelets within pump oxygenator circuits [12,13], and, even more important, platelet dysfunction [2,[13][14][15]] play a central role in the pathogenesis of haemorrhagic complications after ECC.…”

Section: Discussionmentioning

confidence: 99%

“…However, data about acquired platelet abnormalities are controversial. CPB causes prolongation of bleeding time and reduced agglutination, secretion and aggregation [13][14][15][16]. Flow cytometric analysis of different platelet receptors reveales no uniform pictures, decreased [13,17,18], unchanged [19] or increased [20] GPIb expression, decreased [18] or unchanged [13,19] GPIIb-IIIa expression, and increased [13] or unchanged [18,19] numbers of activated circulating platelets having been found during ECC.…”

Section: Discussionmentioning

confidence: 99%

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Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation

Keh

Gerlach

Kürer

et al. 1999

Eur J Clin Investigation

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation

Keh

Gerlach

Kürer

et al. 1999

Eur J Clin Investigation

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“…CPB produces defects in hemostasis associated with reductions in PLT number, 42,46‐50 PLT size, 51‐55 and plasma‐clotting proteins; 33,35,56‐58 acquired PLT dysfunction; 43,59‐66 increased fibrinolytic activity; 36,37,67‐69 inadequate or excessive heparinization; and inadequate or excessive protamine neutralization. Several mechanisms have been suggested as the source of PLT dysfunction after CPB 42,43,59‐66 . We studied the effects of skin temperature on PLT function during and after CPB.…”

Section: The Effect Of Skin Temperature On Plt Function In Extracorpomentioning

confidence: 99%

Nonsurgical bleeding diathesis in anemic thrombocytopenic patients: role of temperature, red blood cells, platelets, and plasma‐clotting proteins

2007

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Research at the Naval Blood Research Laboratory (Boston, MA) for the past four decades has focused on the preservation of red blood cells (RBCs), platelets (PLTs), and plasma-clotting proteins to treat wounded servicemen suffering blood loss. We have studied the survival and function of fresh and preserved RBCs and PLTs and the function of fresh and frozen plasma-clotting proteins. This report summarizes our peer-reviewed publications on the effects of temperature, RBCs, PLTs, and plasma-clotting proteins on the bleeding time (BT) and nonsurgical blood loss. The term nonsurgical blood loss refers to generalized, systemic bleeding that is not corrected by surgical interventions. We observed that the BT correlated with the volume of shed blood collected at the BT site and to the nonsurgical blood loss in anemic thrombocytopenic patients after cardiopulmonary bypass surgery. Many factors influence the BT, including temperature; hematocrit (Hct); PLT count; PLT size; PLT function; and the plasma-clotting proteins factor (F)VIII, von Willebrand factor, and fibrinogen level. Our laboratory has studied temperature, Hct, PLT count, PLT size, and PLT function in studies performed in non-aspirin-treated and aspirin-treated volunteers, in aspirin-treated baboons, and in anemic thrombocytopenic patients. This monograph discusses the role of RBCs and PLTs in the restoration of hemostasis, in the hope that a better understanding of the hemostatic mechanism might improve the treatment of anemic thrombocytopenic patients. Data from our studies have demonstrated that it is important to transfuse anemic thrombocytopenic patients with RBCs that have satisfactory viability and function to achieve a Hct level of 35 vol percent before transfusing viable and functional PLTs. The Biomedical Excellence for Safer Transfusion (BEST) Collaborative recommends that preserved PLTs have an in vivo recovery of 66 percent of that of fresh PLTs and a life span that is at least 50 percent that of fresh PLTs. Their recommendation does not include any indication that preserved PLTs must be able to function to reduce the BT and reduce or prevent nonsurgical blood loss. One of the hemostatic effects of RBC is to scavenge endothelial cell nitric oxide, a vasodilating agent that inhibits PLT function. In addition, endothelin may be released from endothelial cells, a potent vasoconstrictor substance,to reduce blood flow at the BT site. RBCs, like PLTs at the BT site, may provide arachidonic acid and adenosine diphosphate to stimulate the PLTs to make thromboxane, another potent vasoconstrictor substance and a PLT-aggregating substance. At the BT site, the PLTs and RBCs are activated and phosphatidyl serine is exposed on both the PLTs and the RBCs. FVa and FXa, which generate prothrombinase activity to produce thrombin, accumulate on the PLTs and RBCs. A Hct level of 35 vol percent at the BT site minimizes shear stress and reduces nitric oxide produced by endothelial cells. The transfusion trigger for prophylactic PLT transfusion should consider both the H...

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“…Some key aspects affecting the hemostatic system following exposure to CPB include: hypothermia, hemodilution, contact activation, platelet activation and resultant dysfunction, fibrinolysis, and pharmacologic (Heparin, Protamine, etc.) [Wenger et al, 1989;Khuri et al, 1995;Hyde et al, 1998;Muriithi et al, 2000;Murphy and Angelini, 2004;Paparella et al, 2004;Spiess et al, 2004;McGrath et al, 2008]. Each of these can cause various effects on different patients highlighting the importance of individualized risk identification and therapy.…”

Section: Introductionmentioning

confidence: 99%

Point of Care Testing in Cardiac Surgery: Diagnostic Modalities to Assess Coagulation and Platelet Function

Stafford

Weitzel

2013

Drug Development Research

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Point of Care testing in the perioperative arena is a high priority topic, specifically in cardiac surgery where a majority of perioperative blood transfusions occur. Platelet function in particular is of interest in cardiac surgery as cardiopulmonary bypass itself creates known platelet dysfunction, but also because more and more patients are on antiplatelet agents due to coronary stenting procedures. This review will focus on presenting current data relating to platelet function in the perioperative setting, along with a brief review of general coagulation concepts. Drug Dev Res 74 : 418-427, 2013.

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Loss of platelet fibrinogen receptors during clinical cardiopulmonary bypass

Cited by 150 publications

References 18 publications

Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation

Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation

Nonsurgical bleeding diathesis in anemic thrombocytopenic patients: role of temperature, red blood cells, platelets, and plasma‐clotting proteins

Point of Care Testing in Cardiac Surgery: Diagnostic Modalities to Assess Coagulation and Platelet Function

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