veratrine/bjúgur

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[Inhibition of veratrine-induced pulmonary edema in the guinea pig by dehydrated ergot alkaloids (hydergin)].

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Mechanisms of intracisternal veratrine pulmonary edema.

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[Changes in the relation between plasma and blood corpuscles during veratrine-pulmonary edema in rabbit].

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Pulmonary vasoconstriction in a canine model of neurogenic pulmonary edema.

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The intracisternal administration of veratrine to the chloralose-anesthetized dog produces pulmonary hypertension (PH) and neurogenic pulmonary edema (NPE). To determine whether pulmonary vasoconstriction, mediated by a circulating agent, contributes to the PH, the left lower lung lobe (LLL)

Analysis of airway fluid protein concentration in neurogenic pulmonary edema.

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Intracisternal administration of veratrine (40 micrograms/kg) in the alpha-chloralose-anesthetized dog produces fulminant neurogenic pulmonary edema (NPE). To determine whether the edema resulted from increased microvascular pressure or from increased permeability, the airway fluid-to-plasma protein

A canine model of neurogenic pulmonary edema.

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The purpose of this study was to evaluate the usefulness of the intracisternal administration of veratrine as a model of neurogenic pulmonary edema (NPE) in the alpha-chloralose-anesthetized dog. Veratrine (40-60 micrograms/kg) was injected into the cisterna magna of 17 animals, and systemic

Adrenal epinephrine increases alveolar liquid clearance in a canine model of neurogenic pulmonary edema.

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Case reports of neurogenic pulmonary edema (NPE) often indicate that the edema resolves quickly. Because plasma epinephrine concentration may be elevated in NPE, and epinephrine has been shown to increase the rate of alveolar liquid clearance (ALC), we determined if ALC was increased in a canine

Edema development and recovery in neurogenic pulmonary edema.

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We determined the time course of changes in extravascular lung water (EVLW) that occur after massive sympathetic activation produced by intracisternal veratrine administration in chloralose-anesthetized dogs. Three groups of dogs were studied. In the first group (n = 9), acute increases in EVLW

Excessive sympathetic nervous system activity decreases myocardial contractility.

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The objective of this study was to determine whether myocardial contractility is depressed by intense activation of the sympathetic nervous system. A massive sympathetic discharge was produced by injecting veratrine or sodium citrate into the cisterna magna of anesthetized rabbits (n = 10). Two and

Circulating neuropeptide Y does not produce pulmonary hypertension during massive sympathetic activation.

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We tested the possibility that neuropeptide Y (NPY) may contribute to the pulmonary hypertension that occurs after massive sympathetic activation produced by intracisternal veratrine administration in the chloralose-anesthetized dog. In six dogs, veratrine caused arterial NPY-like immunoreactivity

Role of EDRF in the cardiopulmonary dysfunction produced by massive sympathetic activation.

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This study was undertaken to determine whether endothelium-derived relaxing factor (EDRF) modulates the pulmonary and systemic hemodynamic responses to massive sympathetic nervous system (SNS) activation and, in so doing, also modulates the degree of SNS-induced left ventricular (LV) dysfunction and

Oxygen consumption after massive sympathetic nervous system discharge.

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We evaluated the possibility that massive, sympathetic nervous system (SNS) activation [as may precede the development of neurogenic pulmonary edema (NPE)] increases O2 demand. O2 consumption (VO2) and plasma concentrations of the calorigenic agents, epinephrine (EPI) and norepinephrine (NE) were

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