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asthma/edema

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[Cardiogenic pulmonary edema following β2 agonist infusion for acute, severe asthma].

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We report the case of a severe acute pulmonary edema secondary to the administration of salbutamol to a patient admitted for severe asthma. The diagnosis of acute pulmonary edema was suspected on the clinical examination, chest radiography, biological (plasmatic Pro-BNP rate) and echocardiographic

Evaluation of blood vessels and edema in the airways of asthma patients: regulation with clarithromycin treatment.

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BACKGROUND Although airway angiogenesis and edema have been proposed to contribute to the airway remodeling process in patients with asthma, there are few studies looking at these structural components in the airway tissue of asthma patients. Mycoplasma infection may be associated with chronic

Pulmonary edema after electroconvulsive therapy in a patient treated for long-standing asthma with a beta2 stimulant.

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A 68-year-old man was scheduled to receive 8 treatments of electroconvulsive therapy (ECT) for severe depression. He was being treated for long-standing asthma with a beta2 stimulant, clenbuterol hydrochloride, and had experienced no asthma attack for 9 years. Although he experienced no adverse

[A case of severe asthma exacerbation complicated with cerebral edema and diffuse multiple cerebral micro-bleeds].

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A 36-year-old woman was admitted to the Intensive Care Unit for the treatment of severe asthma exacerbation. Her condition of asthma improved with systemic glucocorticosteroids, inhaled beta2-agonist, intravenous theophylline and inhaled anesthesia (isoflurane) under mechanical ventilation. Her

Placental growth factor contributes to bronchial neutrophilic inflammation and edema in allergic asthma.

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Placental growth factor (PlGF) and its receptor vascular endothelial growth factor receptor 1 (VEGFR1) play an important role in pathological conditions related to angiogenesis, vascular leakage, and inflammation. This study investigated their contributions to inflammation and the formation of edema

Hypercapnic cerebral edema presenting in a woman with asthma: a case report.

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BACKGROUND Common causes of non-traumatic acute cerebral edema include malignant hypertension, hyponatremia, anoxia, and cerebral vascular accident. The computed tomographic images and data obtained during care of the patient described in this case report provide evidence that hypercarbia can cause

[Therapeutic use of nitroglycerin in pulmonary edema and cardiac asthma in myocardial infarct patients].

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The effect of sublingual medication with nitroglycerin taken in a dose of 0.5-1 mg was studied in 101 patients with myocardial infarction (77 had pulmonary edema and 34 had cardiac asthma). In patients with edema of the lungs nitroglycerin reduced dyspnoea, in some cases of cardiac asthma it
Ovalbumin (OVA)-induced asthma in mouse lungs causes changes in the mRNA and protein levels of aquaporins (AQPs). AQP expression was examined in the presence of various anti-asthmatic agents, including dexamethasone, ambroxol, and terbutaline. The influence of these agents on OVA-induced airway
BACKGROUND Natural products are considered as an essential source for the search of new drugs. Pistacia integerrima galls (PI) have been used for the treatment of asthma and cough in traditional system of medicine. OBJECTIVE Current study investigates the immunomodulatory and anti-inflammatory

[Mechanisms of bronchial hyperreactivity. Bronchial edema, mechanical and vascular factors].

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Hindrance to gas flow in the bronchi is affected not only by airway smooth muscle tone but also by airway circulation. Congestion and oedema increase airway wall thickness and act in series with airway smooth muscle contraction to reduce airway calibre, an effect which is more marked in small and

Dissociation between LPS-induced bronchial hyperreactivity and airway edema in the guinea-pig.

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The interactions between LPS-induced bronchial hyper-reactivity (BHR) and lung inflammation (LI) were investigated. LPS-induced LI was assessed with the augmented alveolo-capillary permeability (ACP) and with the increased migration of neutrophils into the broncho-alveolar lavage fluid. BHR was

[Acute pulmonary edema and cardiac asthma].

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BILATERAL STELLATE GANGLION BLOCK IN CARDIAC ASTHMA AND PULMONARY EDEMA.

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