DDAVP Infusion Does Not Affect Plasma Levels of Endothelin-1 in Four Normal Subjects

Marasini, Bianca; Cugno, Massimo; Bassani, Cristina; Fabrizi, I.; Bottasso, B.; Agostoni, A

doi:10.1055/s-0038-1646329

Cited by 1 publication

(2 citation statements)

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“…It is well known that desmopressin induces the release of vWF and t-PA from endothelial cells when administered in humans (17,21). Venous occlusion does provoke the release of fibrinolytic activators (t-PA and u-PA) from endothelial cells, suggesting that this release is not linked to other secretion pathways, or the release is due to the local hypoxemia produced by the venous stasis because of the minimal damage sufficient to provoke thrombus formation [indicated by the increase of ATM and the cross-linked fibrin degradation product (22)] and can induce the release of the plasminogen activators.…”

Section: Resultsmentioning

confidence: 99%

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Changes in Clotting and Fibrinolytic Parameters Produced by Venous Stasis

Altman

Scazziota

Rouvier

1996

Clin Appl Thromb Hemost

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Vascular endothelial cells have thrombosisprevention properties through the release of some fibrinolytic factors. This capacity of endothelium was studied using the venous occlusion test (VOT) and measuring proteins released during stasis. Blood samples were collected before and after 10 and 20 min VOT in tubes containing sodium citrate at pH 7.0 or 4.3. A significant shortening of the euglobulin clot lysis time (ECLT) was obtained 10 and 20 min after VOT in plasma collected in citrate pH 7.0 or 4.3. No statistical difference was noted between results obtained 10 and 20 minutes after VOT.The shortening was related to the increase of tissue plasminogen activator (t-PA) released during VOT. No difference was detected in the concentration of tissue plasminogen activator inhibitor 1 (PAI-1), but PAI-1 activity measured in plasma from blood collected in citrate pH 7.0 decreased progressively from 10.8 ± 9.2 arbitrary units (AU)/ml to 3.76 ± 4.5 AU/ml and 0.8 ± 1.02 AU/ml (p < 0.001) after 10 and 20 min, respectively, of stasis. When the PAI-1 activity was determined in blood collected in citrate pH 4.3 for preventing in vitro complexing of PAI-1 and t-PA, results were different: PAI-1 activity decreased from a basal value of 29.2 ± 15.3 AU/ml to 24.9 ± 12.2 ( p = NS) and 18.7 ± 11.5; p < 0.02) 10 and 20 min after VOT. As result of fibrinolytic activation, other factors were modified: increase of plasminogen activators, decrease of plasminogen, and increase of D-dimer. Fibrinogen, fibronectin, protein C, protein S, von Willebrand factor, and tissue factor pathway inhibitor concentration remained unchanged after VOT. According to our findings, VOT can be performed with a stasis of 10 min. Good responders are related to the endothelial capacity for releasing t-PA and urokinase-type PA (u-PA) and defined as those with an ECLT of <60 min after 10 min VOT when blood was collected in sodium citrate pH 7.0.

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Section: Resultsmentioning

confidence: 99%

“…Release of proteins from endothelial cells can be obtained by a variety of agents: desmopressin (15)(16)(17), exercise (18), and venous stasis (2,3,(5)(6)(7)19).…”

Section: Resultsmentioning

confidence: 99%