Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pneumothorax, pneumomediastinum and subcutaneous emphysema are potential complications of a variety of pediatric illnesses. A review by the authors confirms the reports of others that asthma is the primary medical cause of pneumothorax and subcutaneous emphysema and that a variety of inflammatory and obstructive lesions can be associated with extra-vasation of pulmonary air. Pneumothorax infrequently complicates asthma. Asthma-associated pneumomediastinum rarely requires vigorous therapeutic intervention and massive subcutaneous emphysema may necessitate tracheostomy. Pressurized delivery of sympathomimetic aerosols have been condemned by some as an unnecessary cause of iatrogenic air leak. The data of the authors indicate that this form of therapy rarely causes air leak syndromes. The pathophysiology of extravasation of pulmonary air is reviewed.
 ...
PMID:Air leak syndromes as complications of respiratory disease in infancy and childhood. 59 76

Spirometric examinations are suitable for the diagnosis of airway obstruction, but not of pulmonary emphysema. Whole body plethysmography, in contrast, is the most reliable diagnostic procedure for both conditions, both qualitatively and quantitatively. The basic treatment of any form of airway obstruction consists in the inhalation of beta-2-sympathomimetic drugs; theophyllines are also good bronchodilators, but are less powerful than beta-2-sympathomimetics. Glucocorticoids must always be given when bronchitis also presents, which is only rarely treatable with antibiotics alone. Although regression of pulmonary emphysema is not possible, progression of the destructive process would appear to be inhibited by intensive treatment of the inflammatory bronchitis. Only in the case of patients with congenital alpha-1-antitrypsin deficiency is it possible to administer such causal treatment in the form of substitution therapy. Surgical treatment can be considered only in the case of bullous pulmonary emphysema.
 ...
PMID:[Obstructive airway diseases--emphysema. Diagnosis and therapy]. 219 Aug 96

Beta 2-adrenergic agents are useful in the management of acute and chronic asthma. Chronic bronchitis and emphysema are less responsive to bronchodilator therapy; however, a trial of beta 2-agonists is warranted in search of a reversible component. The newer beta 2-sympathomimetic agents have no important differences in the quality of bronchodilation, but individual patients may respond more favorably to one drug than to another. Most of the common adverse effects (eg, tremor and tachycardia) are an extension of the pharmacologic effects, so there are no important differences at equipotent doses. When chronic symptoms necessitate maintenance treatment, the frequency of dosing may become a deciding factor in the selection of a bronchodilator. Since tulobuterol is recommended for twice-a-day dosing, it may be more convenient for the patient than beta 2-sympathomimetics that require more frequent administration. The prolonged duration of action of tulobuterol minimizes the need for nocturnal drug administration, allowing the patient to sleep through the night. Thus tulobuterol offers the benefits of extended symptomatic protection and improved patient compliance.
 ...
PMID:Tulobuterol in the management of obstructive airways disease in adults. 286 99

Many studies have evaluated the efficacy of ipratropium bromide in chronic obstructive pulmonary disease (COPD). Single-agent studies have shown ipratropium to be both safe and effective in COPD. Several studies have compared ipratropium with sympathomimetic agents or methylxanthines in patients with chronic bronchitis or emphysema; all of these studies have shown at least an equal, and in most instances a superior, bronchodilator action with ipratropium in terms of duration of action as well as peak bronchodilator effect in patients with COPD. In some patients with COPD, beta agonists, theophylline, or corticosteroids may have some additive, but not synergistic, bronchodilator effects when given with ipratropium.
 ...
PMID:Ipratropium bromide in chronic bronchitis/emphysema. A review of the literature. 294 64

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of ipratropium bromide are reviewed. Ipratropium bromide, a synthetic quaternary isopropyl derivative of atropine, interrupts vagally mediated bronchoconstriction by inhibiting the cyclic guanosine 3',5'-monophosphate system at parasympathetic nerve endings. Ipratropium bromide is poorly absorbed after oral and inhaled administration but diffuses rapidly into tissue after i.v. or i.m. administration. The elimination half-life is 3.2-3.8 hours. After inhalation, the drug is eliminated in the urine and feces. The bronchodilatory effect of ipratropium bromide in stable chronic obstructive pulmonary disease appears to be comparable, and may be superior, to that of the beta-sympathomimetic agents. In acute exacerbations, ipratropium bromide is useful but may not be the preferred agent because of a delayed onset of action (within 15 minutes; mean dose-dependent duration of effect, three to five hours). Combination therapy with other bronchodilating drugs has proved useful. Ipratropium bromide may be a useful adjunctive agent in the treatment of asthma. Since the onset of action is delayed, ipratropium bromide should not be used as single-drug therapy in an acute asthmatic exacerbation. Reported adverse effects, including cough, nausea, palpitations, dry mouth, nervousness, gastrointestinal distress, and dizziness, have been mild. The usual dosage is two inhalations (36 micrograms) four times daily, and the maximum number of doses per day should not exceed 12. Although ipratropium bromide is currently indicated only for maintenance therapy in stable chronic bronchitis and emphysema, it may be useful as adjunctive therapy in asthma and in the management of acute exacerbations of chronic bronchitis and asthma. Additional experience in a variety of chronic obstructive pulmonary disorders will help to clarify the role of ipratropium bromide in the treatment of obstructive pulmonary disease.
 ...
PMID:Use of ipratropium bromide in obstructive lung disease. 297 9

Experiments were designed to investigate whether induced emphysema would lead to pulmonary hypertension and cor pulmonale. Also additional proof was sought on the effect of progestational hormones in preventing the occurrence of emphysema in rats. Measurements of mechanical properties of the lung, of pulmonary circulation and cardiac function of the emphysematous rats were made. To some a solution of .5 ml/100 gm body weight of phytohemagglutinin was injected intratrocheally during the first week and 1 mg/100 gm body weight during the second week. Subcutaneous injections were given daily for 6 weeks. 1 group received .1 ml of .5% methocel. Another group received 5 mg/kg progesterone and a third group, .1 mg/kg medroxyprogesterone. Only about 50% of the rats survived all of these procedures. After 6 weeks the special measurements were made. The functional residual capacity of the group receiving phytohemagglutinin was increased to 4.3 ml compared with 3 ml for control rats with saline injections only and 2.8 ml for the rats with tracheal constriciton only. Also histologic examination of the lungs showed a greater percentage of air spaces in rats having had the combined procedure. This histological change was interpreted as pulmonary emphysema. The protective action of progesterone was based on normal values for functional capactiy (3 ml) and normal values for percentage of air spaces in histologic section of the lung. Both the progesterone and medroxyprogesterone prevented the development of the abnormal functional changes of emphysema. Blood changes determined by catheterization of the carotid artery support the occurrence of lesions which were interpreted as emphysema after the tracheal procedures. Tracheal obstruction was considered responsible for the abnormal values of gas tension in the arterial blood. The emphysematous rats showed higher blood pressures than those without emphysema but values for those with only tracheal obstruction were also higher than controls. The high levels of pulmonary arterial pressure were associated with hypoxia and relieved by inhalation of high oxygen. Cardiac output was diminished in those with as well as those without emphysema. This reduction may be an early functional manisfestation prior to cardiac enlargement and cor pulmonale. Rats with tracheal constriction had elevated pulmonary vascular resistance. The only electrocardiographic changes in emphysematous rats were increased height of P waves. Results indicate that the antiemphysematous effect of progesterone is not exerted on the cardiopulmonary system. The reactivity of the bronchial musculature is not affected. The administration of sympathomimetic bronchodilators does not prevent the appearance of emphysema.
 ...
PMID:Cardiopulmonary effects of progestational agents in emphysematous rats. 508 36

Pulmonary function can be reduced by beta-blockers. It has been established that no beta-blocker is entirely safe in patients with chronic obstructive lung disease. An alternative medication not expected to influence pulmonary function should first be considered. This side effect of beta-blockers develops mostly in patients with reversible bronchial obstruction, and it is much less pronounced in those with irreversible bronchial obstruction. Translated into terms of clinical diagnosis, this means that problems should be expected in patients with bronchial asthma and with asthmatic bronchitis, whereas those with chronic bronchitis and emphysema are much less likely to develop relevant symptoms. It has been demonstrated that beta-blockers with intrinsic sympathomimetic activity (ISA), such as pindolol, and beta 1-selective blockers have a less marked effect on pulmonary function than nonselective beta-blockers without ISA, such as propranolol. The untoward effect can be compensated by combination with a beta-mimetic agent; this mechanism is most effective during beta 1-selective blockade.
 ...
PMID:beta-Adrenoceptor blockade and pulmonary function in patients suffering from chronic obstructive lung disease. 618 19