ouabain/hemorrhage

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Plasma levels of an ouabain-like factor associated with an increased incidence of cerebral haemorrhage in one-kidney, one wrap hypertension in rabbits.

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To examine the role of an ouabain-like factor (OLF) in the pathogenesis of cardiovascular disease in hypertension, we examined plasma levels of OLF in a malignant form of one-kidney, one wrap (1K,1W) hypertension. Two weeks after the induction of hypertension plasma OLF increased to 282% compared to

The effect of ouabain on cardiac performance in experimental hemorrhagic shock.

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Ouabain is secreted by the adrenal gland in awake dogs.

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Ouabain has been identified in the plasma and adrenal glands of several mammals, including humans. To investigate possible adrenal secretion of ouabain in vivo, at rest, and in response to acute blood volume changes, we prepared trained adult dogs (n = 10) with splenectomy and unilateral adrenal

Digoxin antibody decreases natriuresis and diuresis in cerebral hemorrhage.

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OBJECTIVE Brain-damaged patients may develop hyponatremia and natriuresis. Clinical evidence of digoxin antibody effect on natriuresis we found in an 11-year-old boy who developed excessive natriuresis and hyponatremia after brain tumor excision. To better understand the mechanisms involved in these

Altered membrane properties of cerebral vascular smooth muscle following subarachnoid hemorrhage: an electrophysiological study. I. Changes in resting membrane potential (Em) and effect on the electrogenic pump potential contribution to Em.

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Subarachnoid hemorrhage was produced experimentally in cats by intracisternal injection of non-heparinized autologous arterial blood obtained by cardiac puncture under ketamine and xylazine anesthesia. Cats were sacrificed at varying time intervals between 30 min and 7 days post ictus. Measurements

Plasma and cerebrospinal fluid endogenous digoxin-like immunoreactivity in patients with aneurysmal subarachnoid haemorrhage.

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Recent evidence indicates the presence of naturally occurring digitalis-like compounds in mammals, collectively known as either digitalis-like (DLF) or ouabain-like (OLF) factors, presumed to be endogenous hormones regulating the biological activity of the NA+/ K(+)-ATPase and its isoforms. This

Ouabain prevents loss of autoregulation in rat pial arterioles caused by reoxygenation after a brief hypoxic episode.

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Pial arteriolar diameter changes inversely with changes in systemic arterial blood pressure. Such changes are consistent with autoregulatory functions. These responses are reduced by a brief period of hypoxia followed by reoxygenation. By using an open cranial window preparation we assessed the

Digoxin antibody prevents cerebral hemorrhage-induced hypertension.

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BACKGROUND Brain injury may induce hypertension. Because serum ouabain-like compound (OLC) has vasoconstrictor activity, digoxin antibody antihypertensive effects were evaluated using an intracerebroventricular (ICV) hemorrhage rat model. METHODS Four ICV infused Wistar rat groups were studied:

Purine nucleosides stimulate Na/K ATPase, and prolong survival in hemorrhagic shock.

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BACKGROUND Hemorrhagic shock leads to the appearance of substances in plasma that depress Na/K ATPase activity leading to a rise in plasma potassium. Recently, we reported that adenosine can stimulate Na/K ATPase activity, lower the plasma potassium back to control and prolong survival in shocked

Adenosine stimulates NA/K ATPase and prolongs survival in hemorrhagic shock.

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BACKGROUND Hemorrhagic shock leads to the appearance of substances in plasma that can change Na/K ATPase activity. Our laboratory has reported the existence of a plasma inhibitor of Na/K ATPase that appears during shock. Recently, we have isolated a substance in plasma that stimulates Na/K

Adrenergic antagonists reduce lactic acidosis in response to hemorrhagic shock.

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BACKGROUND Hemorrhagic shock is associated with lactic acidosis and increased plasma catecholamines. Skeletal muscle increases lactate production under aerobic conditions in response to epinephrine, and this effect is blocked by ouabain, a specific inhibitor of the cell membrane Na+/K+ pump. In this

Increased skeletal muscle Na+, K+-ATPase activity as a cause of increased lactate production after hemorrhagic shock.

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BACKGROUND Lactate production after hemorrhagic shock may be produced by aerobic glycolysis, which has been linked to activity of the Na+/K+ pump in smooth muscle and other tissues. We tested whether increased muscle Na+/K+ pump activity after shock was linked to increased lactate

Adrenergic blockade reduces skeletal muscle glycolysis and Na(+), K(+)-ATPase activity during hemorrhage.

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BACKGROUND Recent evidence suggests that hyperlactatemia in shock may reflect accelerated aerobic glycolysis linked to activity of the Na(+), K(+)-ATPase rather than hypoxia. Epinephrine stimulates glycolysis in resting muscle largely by stimulating Na(+), K(+)-ATPase activity. This study evaluates

LK sheep reticulocytosis: effect of anti-L on K influx and in vitro maturation.

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After massive hemorrhage, adult sheep with genotypically low potassium (LK) red cells temporarily produce high potassium (HK) cells with ouabain-sensitive K+ pump fluxes equivalent to mature HK red cells. In light of recent reports of different red cell volume populations accompanying the HK-LK

Increased cation permeability in mutant mouse red blood cells with defective membrane skeletons.

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Cellular cation homeostasis in mouse erythrocytes with defective membrane skeletons was examined in three mouse mutants, hemolytic anemia (sphha/sphha), spherocytosis (sph/sph), and normoblastosis (nb/nb), and compared with reticulocytes produced by repetitive bleeding of congenic normal mice. To

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