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noradrenaline/edema

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In the isolated perfused hind legs of rats with enemas induced by carrageenin, dextran or Freund's adjuvant in both paws, resting perfusion pressure was slightly increased whereas the vasopressor action of noradrenaline, lysine-vasopressin and prostaglandin F2 alpha, was decreased. Admixture of

Magnetic resonance relaxation times in acute hydrostatic pulmonary edema induced by noradrenaline in rats.

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Models of pulmonary edema have been used to study the nuclear magnetic resonance (NMR) characteristics of lung water. Several investigators have measured changes in the relaxation times in the permeability type of pulmonary edema, but relatively few have measured relaxation times in the hydrostatic

[Effects of obsidan on the development of pulmonary edema and hemodynamics of the lesser circulation after administration of noradrenaline].

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In experiments on white rats, guinea pigs and cats it was shown that preliminary infusion of propranolol sharply increases the edemagenous lungs sensitiveness to the infusion of exogenous norepinephrine of white rats and guinea pigs. The infusion of the propranolol to cats leads to a decrease of

Effects of intraventricular noradrenaline on vasogenic edema.

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Possible increased risk of pulmonary edema in patients with hepatorenal syndrome on adding octreotide to albumin / noradrenaline therapies.

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[The effect of the delta sleep-inducing peptide on the development of toxic brain edema-swelling].

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Antiedematic effects of the drugs are connected with their action on the mediator systems. DSIP has a wide range of modulatory effects on the brain mediator systems. DSIP antiedematic effect was studied on the toxic brain edema-swelling (BES) model. Physical characteristics of the nervous tissue
Cerebral microvessels receive a noradrenergic innervation originating from the locus coeruleus. Previously, many studies have tried to elucidate the role of the central noradrenergic innervation on the blood-brain barrier (BBB). Many of them are based on chemical destruction of the innervation by

Loss of noradrenaline transporter sites in frontal cortex of rats with acute (ischemic) liver failure.

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There is increasing evidence that central noradrenaline (NA) transport mechanisms are implicated in the central nervous system complications of acute liver failure. In order to assess this possibility, binding sites for the high affinity NA transporter ligand [3H]-nisoxetine were measured by

Pulmonary edema and ascorbic acid loss.

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Loss of ascorbic acid from lung and pulmonary edema were produced in mice by intravenous injection of either adrenaline or noradrenaline (5 mumol/kg). While adrenalectomy performed before noradrenaline administration reduced the degree of pulmonary edema, a prior dose of hexamethonium accentuated

Pheochromocytoma presenting as life-threatening pulmonary edema.

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Acute cardiogenic pulmonary edema as the first presentation of pheochromocytoma is uncommon and usually rapidly fatal. A 39-yr-old man presented in acute cardiogenic shock with global ventricular dysfunction that required high-dose iv inotrope support and an intraaortic balloon pump assist device.

[Effects of a membrane modulator derived from 3-hydroxypyridine class on the development of pulmonary edema].

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The experiment on white rats has revealed that water-soluble antioxidant-emoxipin, having obvious membrane modulating effect, does not influence the rate of watering and congestion of the lungs, the speed of reabsorption of fluid from lung tissue, the permeability of the capillary-alveolar barrier

[Pulmonary expansion edema during the management of a spontaneous pneumothorax. Report of one case].

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Pulmonary expansion edema is a rare complication of the management of primary spontaneous pneumothorax. We report a 20 year old male admitted with a right primary spontaneous pneumothorax. A chest tube connected to a water seal was placed, achieving lung expansion. Immediately, the patient presented

Catecholamine excretion in "idiopathic" edema: decreased dopamine excretion, a pathogenic factor?

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In 16 women with idiopathic edema, urinary dopamine excretion was decreased when compared to control women (146 +/- 13 SE ng/ml/m2 vs. 212 +/- 32, P less than 0.05 in the supine position and 140 +/- 9 vs. 199 +/- 20, P less than 0.005 combined values of supine and recumbent positions) and was also

Exogenous interleukin-6, interleukin-13, and interferon-γ provoke pulmonary abnormality with mild edema in enterovirus 71-infected mice.

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BACKGROUND Neonatal mice developed neurological disease and pulmonary dysfunction after an infection with a mouse-adapted human Enterovirus 71 (EV71) strain MP4. However, the hallmark of severe human EV71 infection, pulmonary edema (PE), was not evident. METHODS To test whether EV71-induced PE

Mast cells contribute to Enterovirus 71 infection-induced pulmonary edema in neonatal mice.

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Enterovirus (EV) 71 infection has been widely acknowledged as the leading cause of severe hand, foot and mouth disease (HFMD), which may rapidly lead to fatal pulmonary edema. In this study, we established a mouse model for EV71 infection exhibiting high incidence of severe symptoms with pulmonary
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