Systemic inflammation increases shear stress‐induced platelet plug formation measured by the PFA‐100

Homoncik, Monika; Blann, Andrew D.; Hollenstein, Ursula; Pernerstorfer, Thomas; Eichler, Hans‐Georg; Jilma, Bernd

doi:10.1111/j.1365-2141.2000.02473.x

Cited by 16 publications

(29 citation statements)

References 10 publications

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“…As previously published [26][27][28], peak VWF levels inversely correlated with nadir values of CEPI-CT (r ¼ )0.56, P < 0.05).…”

Section: Effect Of Endotoxin On Rotemsupporting

confidence: 83%

“…There was neither a change in the time course nor compared with placebo. These results are in contrast to the effects of endotoxemia on the closure time measured with the PFA-100 device [26]. LPS-infusion significantly decreased CEPI-closure time by approximately 50% to reach minimum levels after 4 h [80 s (95%CI 73-88)]; P < 0.05 vs. baseline and placebo).…”

Section: Effect Of Endotoxin On Rotemcontrasting

confidence: 61%

“…These results are in contrast to the effects of endotoxemia on the PFA-100 closure times (CEPI-CT) [26] (Fig. 2).…”

Section: Discussionmentioning

confidence: 56%

“…Twenty healthy male volunteers [aged 26 years (95% CI [22][23][24][25][26][27][28][29]] participated in a placebo-controlled trial. The control group consisted of four volunteers (4:1 randomization).…”

Section: Methodsmentioning

confidence: 99%

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Validation of rotation thrombelastography in a model of systemic activation of fibrinolysis and coagulation in humans

Spiel

Mayr

Firbas

et al. 2006

Journal of Thrombosis and Haemostasis

147

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Summary. Background: Thrombelastography (TEG) is a whole blood assay to evaluate the viscoelastic properties during blood clot formation and clot lysis. Rotation thrombelastography (e.g. ROTEM Ò ) has overcome some of the limitations of classical TEG and is used as a point-of-care device in several clinical settings of coagulation disorders. Endotoxemia leads to systemic activation of the coagulation system and fibrinolysis in humans. Objectives: We validated whether ROTEM Ò is sensitive to endotoxin induced, tissue factor-triggered coagulation and fibrinolysis and if its measures correlate with biohumoral markers of coagulation and fibrinolysis. Patients and methods: Twenty healthy male volunteers participated in this randomized placebo-controlled trial. Volunteers received either 2 ng kg )1 National Reference Endotoxin or saline.Results: Endotoxemia significantly shortened ROTEM Ò clotting time (CT) by 36% (CI 0.26-0.46; P < 0.05) with a strong inverse correlation with the peak plasma levels of prothrombin fragments (F 1 + 2 ) (r ¼ )0.83, P < 0.05). Additionally, endotoxin infusion enhanced maximal lysis (ML) 3.9-fold (CI: 2.5-5.2) compared with placebo or baseline after 2 h (P < 0.05). Peak ML and peak tissue plasminogen activator (t-PA) values correlated excellently (r ¼ 0.82, P < 0.05). ROTEM Ò parameters clot formation time and maximal clot firmness were not affected by LPS infusion, whereas platelet function analyzer (PFA-100) closure times decreased. Conclusions: Rotation thrombelastography (ROTEM Ò ) detects systemic changes of in vivo coagulation activation, and importantly it is a point of care device, which is sensitive to changes in fibrinolysis in humans. The ex vivo measures CT and ML correlate very well with established in vivo markers of coagulation activation (F 1 + 2 ) and fibrinolysis (t-PA), respectively.

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“…As previously published [26][27][28], peak VWF levels inversely correlated with nadir values of CEPI-CT (r ¼ )0.56, P < 0.05).…”

Section: Effect Of Endotoxin On Rotemsupporting

confidence: 83%

Section: Effect Of Endotoxin On Rotemcontrasting

confidence: 61%

“…These results are in contrast to the effects of endotoxemia on the PFA-100 closure times (CEPI-CT) [26] (Fig. 2).…”

Section: Discussionmentioning

confidence: 56%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Validation of rotation thrombelastography in a model of systemic activation of fibrinolysis and coagulation in humans

Spiel

Mayr

Firbas

et al. 2006

Journal of Thrombosis and Haemostasis

147

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“…6,9 One possible reason for marked thrombocytopenia and decreased PCT in response to endotoxin may be that endotoxin induces platelet adhesion and aggregation by increasing the release of various platelet agonists and by stimulating the expression of adhesion molecules on endothelial cells. 1,15,16 Increased rolling and adherence of platelets within liver sinusoids during endotoxemia has been demonstrated, 15 and we previously showed that platelet closure times were shortened in dogs 1 hour after intravenous endotoxin injection. 6,9 Moreover, decreased survival of circulating platelets and increased removal of platelets from circulation due to phagocytosis by the liver macrophages, as described in a rat model, might enhance the severity of thrombocytopenia in dogs with endotoxemia.…”

Section: Discussionmentioning

confidence: 96%

Evaluation of platelet count and its association with plateletcrit, mean platelet volume, and platelet size distribution width in a canine model of endotoxemia

Yılmaz

Eralp

İlçöl

2008

Veterinary Clinical Pathol

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Background: Platelets are of great importance in the pathogenesis of endotoxemia. Although thrombocytopenia is used as a diagnostic sign of endotoxemia, changes in values for platelet indices (plateletcrit [PCT], mean platelet volume [MPV], and platelet size distribution width [PDW]) in response to endotoxin are still unknown. Objective: The aim of this study was to evaluate platelet count and its relations with platelet indices in a canine model of endotoxemia. Methods: Twenty dogs were divided into 2 groups of 10 each, and treated intravenously with Escherichia coli endotoxin (1 mg/kg) or vehicle. Venous blood samples were collected before treatment (0 hour) and 0.5, 1, 2, 4, 6, 8, 12, and 24 hours after treatment. Platelet counts and indices were determined on a CELL-DYN hematology analyzer. Results: The platelet count and PCT decreased by a mean of 73% and 93%, respectively (P o.001), at 0.5 hour, and remained 70% and 85% lower than baseline values (P o.001) for 24 hours after endotoxin injection. MPV and PDW increased by a mean of 28% and 45%, respectively (P o.01), at 0.5 hour, and remained increased by 7% and 16% over baseline values for 24 hours (P o.01-.001). Platelet count correlated positively with PCT (P o.001), but correlated negatively with MPV (P o.001) and PDW (P o.01). Conclusions: Changes in platelet count and its association with platelet indices may reflect changes in platelet production and reactivity. Platelet indices have potential value in the diagnosis and monitoring of dogs and humans with endotoxemia.

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Endotoxaemia modulates Toll‐like receptors on leucocytes in humans

Marsik¹,

Mayr²,

Cardona³

et al. 2003

Br J Haematol

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Summary. The modulation of Toll‐like receptors (TLR) 1, 2 and 4 was studied during experimental human endotoxaemia. Healthy volunteers received 2 ng/kg of lipopolysaccharide (LPS) endotoxin (n = 10). TLR1, 2 and 4 expression occurred on monocytes and neutrophils, with monocytes expressing higher baseline levels of TLR2. LPS infusion downmodulated TLR4 expression on neutrophils, with maximal downregulation occurring at 24 h (−62% from baseline; P < 0·03 versus baseline). Monocyte TLRs were upregulated in vivo (TLR1 and 2), and in vitro (TLR1, 2 and 4) 8 h after LPS bolus (P < 0·05 versus baseline). Therefore, neutrophils and monocytes differentially express surface TLRs, and endotoxaemia differentially regulates TLR expression.

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Systemic inflammation increases shear stress‐induced platelet plug formation measured by the PFA‐100

Cited by 16 publications

References 10 publications

Validation of rotation thrombelastography in a model of systemic activation of fibrinolysis and coagulation in humans

Validation of rotation thrombelastography in a model of systemic activation of fibrinolysis and coagulation in humans

Evaluation of platelet count and its association with plateletcrit, mean platelet volume, and platelet size distribution width in a canine model of endotoxemia

Endotoxaemia modulates Toll‐like receptors on leucocytes in humans

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