adenosine diphosphate/hemorrhage

The effect of intravenous infusion of adenosine diphosphate (ADP) on haemostatic and thrombotic mechanisms was studied in rats and rabbits. Infusion of ADP (0.2-1 microMol/kg/min) in rabbits prolonged the skin capillary bleeding time threefold after between 1/2 and 2 hours of infusion. Prolongation

OBJECTIVE To investigate the association between adenosine diphosphate (ADP)-induced platelet aggregation measured by single-platelet count testing and postoperative blood loss in clopidogrel-treated patients with acute coronary syndromes undergoing coronary artery bypass grafting

The nonpeptide platelet glycoprotein IIb/IIIa antagonist, L-738, 167, was characterized in dog and nonhuman primate. In an anesthetized canine model of coronary artery electrolytic lesion, L-738,167 elicited dose-dependent (3, 4, 4.5 and 5 micrograms/kg i.v.) decreases in incidence of occlusion,

OBJECTIVE To study the effects of poly-adenosine diphosphate ribosyl-polymerase (PARP) on vascular hyporeactivity during hemorrhagic shock in rats. METHODS Sprague-Dawley (SD) rats were randomly divided into three groups: shock, 3-aminobenzamide (3-AB) pretreatment+shock, and sham operation.

Current guidelines recommend adenosine diphosphate receptor inhibitors (ADPRi) be discontinued 5-7 days prior to cardiac surgery due to increased bleeding events, rates of re-exploration, and transfusions. However, the risks of left ventricular assist device (LVAD) implantation in patients taking an

P2Y12, one of the two platelet receptors for adenosine diphosphate (ADP), plays a central role in platelet function. Defects of P2Y12 should be suspected when ADP, even at high concentrations (≥10 µM), is unable to induce full, irreversible platelet aggregation. Patients with congenital P2Y12

Dual antiplatelet therapy with aspirin and a P2Y12 receptor blocker is a key strategy to reduce platelet reactivity and to prevent thrombotic events in patients treated with percutaneous coronary intervention. In an earlier consensus document, we proposed cutoff values for high on-treatment platelet

BACKGROUND Coagulopathy in traumatic brain injury (CTBI) is a well-established phenomenon, but its mechanism is poorly understood. Various studies implicate protein C activation related to the global insult of hemorrhagic shock or brain tissue factor release with resultant platelet dysfunction and

Objectives: To investigate the association of adenosine diphosphate (ADP)-induced platelet maximum amplitude (MA_ADP) with postoperative bleeding and blood product transfusions in patients undergoing coronary artery bypass