Cardiopulmonary bypass induces leukocyte-platelet adhesion

Rinder, CS; Bonan, JL; Rinder, HM; Mathew, Joseph P.; Hines, Robert Stephan; Smith, Bernard

doi:10.1182/blood.v79.5.1201.bloodjournal7951201

Cited by 48 publications

(61 citation statements)

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“…Platelets are activated in patients with SCD (Tomer, Eckman & Vroon, 1992;Tomer, Harker & Eckman, 1994;Browne et al, 1996;Wun et al, 1997Wun et al, , 1998. Activated platelets can bind to and activate monocytes (Silverstein & Nachman, 1987;Rinder et al, 1992;Redlich et al, 1998) and PMAs are likely to play a role in vascular disease (Furman et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Activated monocytes and platelet-monocyte aggregates in patients with sickle cell disease*

et al. 2002

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Tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) increase endothelial surface receptors that mediate the adherence of sickle erythrocytes to the endothelium. Increased circulating levels of these cytokines have been found in patients with sickle cell disease (SCD). Monocytes are a source of both of these inflammatory mediators; we therefore determined whether circulating monocytes were activated in SCD, as defined by intracellular expression of these cytokines. Blood was also assayed for the presence of platelet-monocyte aggregates (PMAs), as platelet adherence is one possible mechanism for monocyte activation. The median percentages of monocytes expressing intracellular TNF-alpha and IL-1beta in SCD patients were 6.8 (2.8-17.3) [median (range)] and 14.1 (1.3-44.8), respectively. In African-American controls the corresponding percentages were 0.3 (0.1-0.5) and 0.4 (0.1-3.0), and in Caucasians 0.2 (0.1-0.5) and 0.8 (0.8-1.9) (P < 0.001, Kruskal-Wallis). The mean percentage (+/- SD) of PMA was 14.0 +/- 8.3 for Caucasian controls, 25.7 +/- 7.3 for African-American controls, and 45.7 +/- 21.6 for patients with SCD (P < 0.001, RM ANOVA; P < 0.05, Newman-Keuls posthoc test). We conclude that there are increased circulating PMAs and monocyte activation in patients with SCD.

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Section: Discussionmentioning

confidence: 99%

Activated monocytes and platelet-monocyte aggregates in patients with sickle cell disease*

et al. 2002

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“…Increased PLA formation has been found in unstable coronary artery disease, 10 myocardial infarction, 21 and cardiopulmonary bypass. 8 However, there are few clinical reports on drug effects on formation of PLA. These data show that aspirin has no effect on PLA formation, 22,23 whereas the thienopyridine ticlopidine, given with aspirin after intracoronary stenting, reduced formation of platelet-monocyte conjugates 46% in association with a 28% decrease in Mac-1 expression on monocytes.…”

Section: Discussionmentioning

confidence: 99%

“…7 Increased formation of PLA has been reported in acute coronary syndromes and cardiopulmonary bypass. [8][9][10] In consequence, formation of PLA has been acknowledged as a possible target for antiaggregatory therapy in acute coronary syndromes and coronary interventions. 11 In vitro studies showed that many different leukocyte types (polymorphonuclear neutrophils, monocytes, and lymphocytes) can bind to activated platelets through leukocyte adhesion molecule P-selectin (CD62), a constituent of platelet granules that is transported to the platelet surface on stimulation with agonists and is generally perceived as a marker of platelet activation.…”

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confidence: 99%

Clopidogrel, but not abciximab, reduces platelet leukocyte conjugates and P‐selectin expression in a human ex vivo in vitro model

Klinkhardt

2002

Clin Pharma and Therapeutics

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Formation of platelet-leukocyte aggregates (PLA) through the CD62 ligand is an important mechanism by which leukocytes contribute to thrombosis and inflammation. We investigated the formation of PLA in human subjects after stimulation with thrombin receptor activating peptide and adenosine diphosphate (ADP) after treatment with clopidogrel and after in vitro application of the platelet glycoprotein IIb/IIIa complex antagonist abciximab. Expression of CD62 was significantly reduced 30% to 50% with clopidogrel, depending on the type and concentration of the inducer, but addition of abciximab led to a significant approximately 30% increase in CD62 expression when platelets were stimulated by ADP. Formation of PLA decreased significantly with clopidogrel to 55% to 75% of the baseline value, whereas addition of abciximab caused a significant increase in PLA in ADP-stimulated samples before but not after administration of clopidogrel. The increase in formation of PLA after in vitro addition of abciximab was not paralleled by a decrease in platelet microaggregates and is therefore presumed not caused by enhanced availability of platelets. To our knowledge, this is the first report showing that clopidogrel reduces formation of PLA. The findings also suggest intersection between an "outside-in" signal generated by abciximab and stimulation of platelet P2T(12) purinergic receptors that augments degranulation and increases formation of PLA but is inhibited by clopidogrel.

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“…A rapid elimination of activated platelets would clearly influence efforts to detect them. The presence of platelets attached to white cells has indeed been shown to be increased during cardiopulmonary bypass [18], and a quantitative evaluation of this interaction needs to be included in future studies. Another important question concerns the definition of platelet activation.…”

Section: Discussionmentioning

confidence: 99%

Markers of platelet activation in coronary heart disease patients

Nurden

Macchi

Bihour

et al. 1994

Eur J Clin Investigation

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We have applied flow cytometry to the detection of activated platelets in patients with coronary heart disease. Paraformaldehyde-fixed platelets were incubated with one of the following monoclonal antibodies (MAbs): Bx-1 (anti-GP Ib), AP-2 (anti-GP IIb-IIIa complex), VH10 (anti-GMP-140, a glycoprotein of the alpha-granule membrane), or PAC-1 (directed against an activation-dependent determinant on GP IIb-IIIa complexes). Bound antibody was quantitated after the addition of FITC-conjugated anti-immunoglobulin. This report highlights studies on 16 unstable angina patients undergoing transluminal angioplasty. Blood samples were taken at different periods before and after the angioplasty. Levels of activated platelets were variable, remaining in the 2-4% range of control donors for some, but increasing to 10-30% post-angioplasty for others (despite all patients receiving heparin and aspirin). Maximum numbers of activated platelets were detected at 24 or 48 h. Nonetheless, the amount of antibody bound to individual platelets rarely reached the levels seen when control platelets were stimulated with thrombin in vitro. Results with VH10 and PAC-1 often, but not always, correlated suggesting different pathways of platelet activation.

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Cardiopulmonary bypass induces leukocyte-platelet adhesion

Cited by 48 publications

References 0 publications

Activated monocytes and platelet-monocyte aggregates in patients with sickle cell disease*

Activated monocytes and platelet-monocyte aggregates in patients with sickle cell disease*

Clopidogrel, but not abciximab, reduces platelet leukocyte conjugates and P‐selectin expression in a human ex vivo in vitro model

Markers of platelet activation in coronary heart disease patients

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