ouabain/edema

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The enhancement of retinal adhesiveness by ouabain appears to involve cellular edema.

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Our previous work showed that ouabain increases retinal adhesion to the retinal pigment epithelium, but the mechanism of this effect has been unclear. In this study, we have found that the ouabain-induced increase in retinal adhesiveness was blocked reversibly by removing sodium from the medium or

The endogenous ouabain-like sodium pump inhibitor in cold injury-induced brain edema.

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An endogenous ouabain-like factor (EOLF) was measured in brain tissue of cats 12 and 24 hrs after cold injury-induced edema. EOLF was assayed via its inhibition of 86Rb+ uptake in human red blood cells in a fraction which was obtained from brain tissue by methanol extraction, chloroform treatment

The effect of intracerebral ouabain administration on the composition of edema fluid isolated from cats with cold-induced brain edema.

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Brain edema fluid was collected from cats with a freezing lesion in the left parietal cortex by the insertion into the brain of needles containing nylon wicks and connected to polyethylene tubes. The edema fluid samples which accumulated in the polyethylene tubes were regularly analyzed for Na+ and

[Electron microscopic study on ouabain-induced brain edema].

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[Biochemical study of brain edema. 3. Experiment on inhibition of Na, K-activated ATPase by ouabain in the brain].

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The effects of ouabain on endothelial function in human and rabbit corneas.

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These experiments were undertaken to study the effects of ouabain on endothelial function in isolated perfused human and rabbit corneas. Both human and rabbit corneas swell at rates which are dose-dependent when perfused with ouabain (10(-8) to 10(-5) M). The human tissue, however, requires tenfold

Endogenous Na/K ATPase inhibitor ouabain in critically ill children with lung injury.

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OBJECTIVE To measure ouabain, an endogenous adrenocortical Na/K ATPase inhibitor, in critically ill children with acute lung injury and relate it to parameters reflecting epithelial sodium transport. METHODS Prospective observational study. METHODS Paediatric Intensive Care Unit of Royal Liverpool

Vasopressin-2 receptor antagonist attenuates the ability of the lungs to clear edema in an experimental model.

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In the last two decades, the role of the alveolar active sodium transport was extensively studied and was found to play a crucial role in regulating alveolar fluid clearance (AFC), and thus in keeping the airspaces free of edema. The recent development of highly selective nonpeptide

[Early tracheal intubation and mechanical ventilation in the treatment of pulmonary edema secondary to ischemic heart disease].

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Forty patients with overt pulmonary edema secondary to ischemic heart disease were treated in the emergency room with iv ouabain and furosemide; 20 patients in Group A received sublingual nifedipine before undergoing early tracheal intubation and mechanical ventilation with 100% FiO2 during 15 min.

Airway surface liquid volume expansion induces rapid changes in amiloride-sensitive Na+ transport across upper airway epithelium-Implications concerning the resolution of pulmonary edema.

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During airway inflammation, airway surface liquid volume (ASLV) expansion may result from the movement of plasma proteins and excess liquid into the airway lumen due to extravasation and elevation of subepithelial hydrostatic pressure. We previously demonstrated that elevation of submucosal

Endogenous ouabain in Ménière's disease.

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OBJECTIVE Endogenous Ouabain (EO) has been demonstrated to modulate the activity of Na+, K+ -ATPase. Our purpose was to measure plasma levels of EO in Ménière's Disease (MD) subjects as a possible predisposing factor to developing and maintaining hydrops. METHODS Case-control

The effect of "ouabain" on the ultrastructure of cerebral arterioles and surrounding tissue, studied by a cannulation of a cerebral artery.

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A technique for cannulation of a parietal branch of the middle cerebral artery is described by which high but local concentrations of substances can be achieved in cortical vessels. Using this technique it was shown that ouabain, a specific inhibitor of the Na+-K+-ATPase enzyme system, can produce

Modifications of synaptosomal Na+ -K+ -ATPase activity during vasogenic brain edema in the rabbit.

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This study investigates the functioning of synaptosomal ouabain-sensitive Na+ -K+ -ATPase in cold-induced edema. During vasogenic brain edema development, the enzyme affinities for Na+ and K+ are progressively decreased paralleling the increase in the tissue water content, whereas maximal velocity

Vascular permeability and epithelial transport effects on lung edema formation in ischemia and reperfusion.

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To determine the role of various Na+ transport systems in the edema fluid accumulation after ischemia and reperfusion in the lung, we evaluated the effect of amiloride (a Na+ channel blocker), ouabain (a Na(+)-K(+)-adenosinetriphosphatase blocker), and phloridzin (a Na(+)-glucose cotransport

Aldosterone regulates Na,K-ATPase and increases lung edema clearance in rats.

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Aldosterone increases the Na,K-ATPase function in renal cells involved in active Na(+) transport. Because the alveolar type 2 (AT2) cells participate in active Na(+) transport, we studied whether aldosterone regulates the Na,K-ATPase in rat AT2 cells and whether aldosterone delivered by aerosols to

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