aminophylline/edema

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Effect of aminophylline on postischemic edema and brain damage in cats.

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We attempted to ameliorate postischemic edema and brain tissue injury in cats by administering aminophylline to reduce the reactive hyperemia that supposedly aggravates both these sequelae. Forty-one cats were subjected to 1 hour of middle cerebral artery occlusion and were killed after 3 hours, 3

Dibutyryl cAMP, aminophylline, and beta-adrenergic agonists protect against pulmonary edema caused by phosgene.

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Phosgene is a toxic oxidant gas that causes the adult respiratory distress syndrome in exposed workers. Phosgene exposure markedly increased lung weight gain in buffer-perfused isolated rabbit lungs (31 +/- 5 g over 60 min after phosgene vs. 7.7 +/- 1.2 in control lungs, P less than 0.01) and

[Hemodynamic effects of aminophylline and nifedipine in patients with high altitude pulmonary edema].

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OBJECTIVE To evaluate the hemodynamic effects of aminophylline and nifedipine in patients with HAPE. METHODS 10 patients with HAPE undergone Swan-Ganz catheter. The parameters of hemodynamics and arterial blood gases in HAPE were measured before and after administration of nifedipine 20 mg

Isoproterenol or aminophylline attenuate pulmonary edema after acid lung injury.

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We tested the hypothesis that isoproterenol and aminophylline would reduce both the pulmonary hypertension and increased pulmonary vascular permeability caused by the intratracheal instillation of hydrochloric acid. The lungs of New Zealand white rabbits were studied using a blood-perfused isolated

Effects of morphine and aminophylline on the severity of obstruction to left ventricular outflow in idiopathic hypertrophic subaortic stenosis: potential adverse effects in treatment of pulmonary edema.

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Theophylline kinetics in acute pulmonary edema.

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Nine patients with acute cardiogenic pulmonary edema were given theophylline intravenously, and its disposition was observed over the next 24 hr. Compared to that in 19 normal subjects, these patients had prolonged plasma half-lifes (mean, 22.9 from 6.7 hr) and decreased plasma clearances of

[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.

Arterial blood gases in acute pulmonary edema.

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Arterial blood gas and pH measurements in 82 patients with acute pulmonary edema of cardiogenic origin entering the emergency department varied widely and were unpredictable using clinical examination. The mean arterial oxygen tension (PaO2) measured in 71 patients breathing room air was 59 mm Hg.

Acute Pulmonary Edema.

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Patients with acute cardiogenic pulmonary edema require rapid assessment and therapy to prevent progression to respiratory failure and cardiovascular collapse. The goal of therapy is to decrease the pulmonary capillary wedge pressure by decreasing intravascular volume and shifting the blood volume

Treatment of acute pulmonary edema.

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When possible, the management of acute cardiogenic pulmonary edema should be started before the patient reaches the hospital. Simple measures such as having the patient sit up with the legs dependent, administering oxygen by nasal prongs, giving sublingual nitroglycerin and small doses of morphine,

Influence of thermal stress and various agents on the brain edema formation in rats following a cryogenic brain lesion.

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The influence of cold stress, heat stress, or various agents on the development of brain edema were assessed in rats following a cryogenic brain lesion. Brain edema was induced by local cold injury to the cortex. Cerebral edema was assessed 0.5, 3.0 or 24 h after a cryogenic brain lesion by

Intravenous nitrates in the prehospital management of acute pulmonary edema.

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OBJECTIVE We sought to assess the effect of nitrates on prehospital mortality among patients with acute pulmonary edema (APE). METHODS The study involved a retrospective evaluation of the records of prehospital outcome in 640 patients with APE rescued by the mobile CCU (MCCU) of Florence, Italy,

Influence of various agents on the development of brain edema in the rat following microembolism. Protective effect of gamma-butyrolactone.

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Brain edema was induced in rats by injecting 50 mu microspheres, labelled with 85Sr, into the internal carotid artery. The use of radioactive microspheres as embolic agents enabled the number of microspheres to be determined in each cerebral hemisphere. Edema was assessed 12 or 24 h after

Inhibition of lipopolysaccharide-induced pulmonary edema by isozyme-selective phosphodiesterase inhibitors in guinea pigs.

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There is a need for pharmacological agents for the treatment of pulmonary edema associated with the adult respiratory distress syndrome. Therefore, we examined the effects of isozyme-selective cyclic AMP phosphodiesterase (cAMP PDE) inhibitors, as well as aminophylline and dexamethasone, on the

[Clarkson syndrome: a rare clinical condition characterized by generalized edema associated to monoclonal gammopathy].

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Generalized edema is commonly due to cardiac failure, renal changes, hepatic and metabolic disturbances, or it can be idiopathic, i.e. primitive lymphedema. Here we describe a patient with several episodes of fluid extravasation characterized by hypotension, hemoconcentration and functional renal

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