anticoagulant/hypoxia

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Hypoxia and the anticoagulants dalteparin and acetylsalicylic acid affect human placental amino acid transport.

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BACKGROUND Anticoagulants, e.g. low-molecular weight heparins (LMWHs) and acetylsalicylic acid (ASA) are prescribed to women at risk for pregnancy complications that are associated with impaired placentation and placental hypoxia. Beyond their role as anticoagulants these compounds exhibit direct

Modulation of endothelial function by hypoxia: perturbation of barrier and anticoagulant function, and induction of a novel factor X activator.

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Exposure of the vessel wall to hypoxemia is a central feature of ischemic cardiovascular disease. This led us to examine the perturbation of endothelial cell properties under hypoxia. An atmosphere of pO2 of 12 mmHg is not lethal to the endothelial cells for up to five days, but barrier function was

High D-dimer levels after stopping anticoagulants in pulmonary embolism with sleep apnoea.

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Obstructive sleep apnoea is a risk factor for pulmonary embolism. Elevated D-dimer levels and other biomarkers are associated with recurrent pulmonary embolism. The objectives were to compare the frequency of elevated D-dimer levels (>500 ng·mL(-1)) and further coagulation biomarkers after oral

Hypoxia/Hypoxemia-Induced activation of the procoagulant pathways and the pathogenesis of ischemia-associated thrombosis.

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Although oxygen deprivation has long been associated with triggering of the procoagulant pathway and venous thrombosis, blood hypoxemia and stasis by themselves do not lead to fibrin formation. A pathway is outlined through which diminished levels of oxygen activate the transcription factor early

Activated protein C attenuates microvascular injury during systemic hypoxia.

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In response to hypoxia, an inflammatory cascade is initiated and microvascular injury ensues. Specifically, within 10 min, leukocyte adherence to the endothelium begins, and leukocyte emigration and vascular leak soon follow. Activated protein C (APC) has been reported to have both anticoagulant and

The effect of hypoxia on capillary endothelial cell function: modulation of barrier and coagulant function.

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As the cells forming the luminal vascular surface, endothelium is exposed to alterations in the vascular microenvironment, such as hypoxaemia. In this report we demonstrate that hypoxia, with pO2 as low as 12-14 mmHg, was not toxic to endothelium, but reversibly modulated central cellular functions

Spontaneous Rupture of a Mediastinal Bronchial Artery Aneurysm Induced by Anticoagulant Agent.

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Nontraumatic spontaneous rupture of a bronchial artery aneurysm is rarely seen. In this report, we described such a phenomenon in a patient induced by usage of anticoagulant agent. The patient had no antecedent history of trauma, hypertension, or apparent aortic pathology. The patient who had been

Cardiopulmonary bypass using argatroban as an anticoagulant for a 6.0-kg pediatric patient.

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A patient was born with transposition of the great arteries, double-outlet right ventricle, interrupted aortic arch, and a ventricular septal defect and underwent a Damus-Kaye-Stansel procedure with a modified Blalock-Taussig shunt at 14 days old. Three months later, this patient presented with

Macrovascular and microvascular endothelium during long-term hypoxia: alterations in cell growth, monolayer permeability, and cell surface coagulant properties.

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In bovine aortic or capillary endothelial cells (ECs) incubated under hypoxic conditions, cell growth was slowed in a dose-dependent manner at lower oxygen concentrations, as progression into S phase from G1 was inhibited, concomitant with decreased thymidine kinase activity. Monolayers grown to

Use of Oral Anticoagulation and Diabetes Do Not Inhibit the Angiogenic Potential of Hypoxia Preconditioned Blood-Derived Secretomes

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Patients suffering from tissue ischemia, who would greatly benefit from angiogenesis-promoting therapies such as hypoxia preconditioned blood-derived secretomes commonly receive oral anticoagulation (OA) and/or have diabetes mellitus (DM). In this study, we investigated the effect of OA

Acquired right-to-left intracardiac shunts and severe hypoxemia.

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Critically ill hypoxemic patients without significant radiological changes on the chest x-ray present a diagnostic and therapeutic problem. Three patients with patent foramen ovale and a patient with a spontaneously closed congenital ventricular septal defect which reopened due to ischemic changes

A prospective multicenter cohort study of the association between global tissue hypoxia and coagulation abnormalities during early sepsis resuscitation.

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OBJECTIVE Coagulation activation is an integral part of sepsis pathogenesis. Experimental data suggest that endothelial exposure to hypoxia activates coagulation. We aimed to test the hypothesis that the quantity of exposure to global tissue hypoxia is associated with the degree of coagulation

[Hypoxemia after heart surgery by a right-left shunt via a permeable unrecognized foramen ovale].

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Hypoxemia is a relatively common complication in the immediate postoperative period after cardiac surgery under cardio-pulmonary bypass, usually due to pulmonary disease. When this does not improve with oxygen therapy and in the absence of pulmonary disease, it may be due to a right-to-left shunt.

[Occult intrapulmonary hemorrhage caused by anticoagulants].

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Intrapulmonary occult bleeding is a serious complication of anticoagulants. Diagnostic difficulties are such that this complication is rarely described: 8 cases in the literature. The authors report two new cases. In both of these patients oral anticoagulant therapy resulted in a severe haemorrhagic

Diagnostic and therapeutic implications of transesophageal echocardiography in medical ICU patients with unexplained shock, hypoxemia, or suspected endocarditis.

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OBJECTIVE To evaluate the diagnostic and therapeutic implications of transesophageal echocardiography (TEE) in intensive care patients. METHODS Comparative study. METHODS A 10-bed general intensive care unit. METHODS Between 1 January 1992 and 31 May 1993, 61 patients prospectively identified with

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