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Atropine may prevent the development of neurogenic pulmonary edema.
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Neurogenic pulmonary edema is an acute life-threatening complication of central nervous system injury. We introduce a hypothesis that early i.v. administration of high-dose atropine can prevent neurogenic pulmonary edema development on the basis of the prevention of baroreflex-induced bradycardia,
[Effect of atropine on development of experimental model of high-altitude acute lung edema].
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[The protective action of high doses of atropine in adrenaline-induced acute pulmonary edema in the rabbit].
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[Effect of a combination of procaine, phenylethylbarbituric acid and atropine on lung edema and bronchospasm in animal experiment and clinical experience. EXPERIMENTAL AND CLINICAL STUDIES ON THE INTRAVENOUS APPLICATION OF A PROCAINE GLUCOSIDE].
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Capsaicin-sensitive nerves exert an inhibitory effect on the development of fibrin-induced pulmonary edema in rats.
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This study was undertaken to evaluate the role of vagal nerves in the development of neurogenic pulmonary edema. We injected fibrinogen and thrombin into the cisterna magna of rats, a model of neurogenic pulmonary edema. When the vagal nerves were left intact, pulmonary edema occurred
[A case of pulmonary edema after electroconvulsive therapy under propofol anesthesia].
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Electroconvulsive therapy (ECT) was scheduled for a 61-yr-old woman with major depression who had been taking a beta-blocker for hypertension. She underwent the first ECT under thiamylal anesthesia uneventfully. The second ECT was performed under propofol anesthesia on the next day. Immediately
Visualization of airway obstruction in vivo during pulmonary vascular engorgement and edema.
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Although pulmonary vascular engorgement has often been hypothesized to decrease airway caliber, leading to airway obstruction in asthma, direct evidence for this hypothesis is lacking. In the present study, we used high-resolution computed tomography to directly measure the changes in the caliber
Altered capillary filtration coefficient in parathion- and paraoxon-induced edema in isolated and perfused rabbit lungs.
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Changes in pulmonary endothelium permeability and in microvascular hemodynamics induced by parathion (Pth) and paraoxon (Pox), its active metabolite, were investigated in isolated, perfused rabbit lungs. Blood-free perfusate was recirculated through isolated and ventilated lungs in an isogravimetric
Neurogenic pulmonary edema induced by spinal cord injury in spontaneously hypertensive and Dahl salt hypertensive rats.
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Neurogenic pulmonary edema (NPE), which is induced by acute spinal cord compression (SCC) under the mild (1.5 %) isoflurane anesthesia, is highly dependent on baroreflex-mediated bradycardia because a deeper (3 %) isoflurane anesthesia or atropine pretreatment completely abolished bradycardia
Prediction of visual acuity recovery in cystoid macular edema.
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Three consecutive patients participated in a prospective evaluation of pseudophakic cystoid macular edema. The duration of the macular edema ranged from 6 to 8 months. On the initial visit, the best corrected acuity with spectacles was determined and a potential acuity meter reading was obtained;
Inhibition of Paf-acether-induced edema of the rat's paw.
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Three classes of drugs were found, after their i.p. administration, to inhibit Paf-acether-induced edema of the rat's paw. These were beta-adrenergic agonists (isoproterenol, salbutamol), alpha-adrenergic antagonists (prazosin, ergotamine, yohimbine, phenoxybenzamine), and calcium entry blockers
EXPERIMENTS ON THE CAUSATION AND AMELIORATION OF ADRENALIN PULMONARY EDEMA.
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The intratracheal injection of one moderate dose of adrenalin in rabbits whose vagi are divided produces a marked pulmonary edema in a large percentage of cases. The same dose in normal animals causes only slight effects. Artificial respiration greatly reduces the production of pulmonary edema in
Hemodynamic mechanisms of neurogenic pulmonary edema.
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Acute lung injury has been reported in man and animals with intracranial disorders, head trauma or cerebral compression. Early studies in our laboratory demonstrated that pulmonary hemorrhagic edema (PHE) of acute and fulminating type occurred accompanying severe hypertension and bradycardia
Aerosolized delivery of oxime MMB-4 in combination with atropine sulfate protects against soman exposure in guinea pigs.
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We evaluated the efficacy of aerosolized acetylcholinesterase (AChE) reactivator oxime MMB-4 in combination with the anticholinergic atropine sulfate for protection against respiratory toxicity and lung injury following microinstillation inhalation exposure to nerve agent soman (GD) in guinea pigs.
Effects of the tripeptide substance P antagonist, FR113680, on airway constriction and airway edema induced by neurokinins in guinea-pigs.
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FR113680 is a newly developed tripeptide substance P (SP) receptor antagonist. The effects of FR113680 on airway constriction and airway edema induced by neurokinins were investigated in guinea-pigs. In in vitro experiments, FR113680 inhibited the contraction of isolated guinea-pig trachea induced
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