Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The substituted benzylamin-derivative fominoben (PB 89 Noleptan) was intravenously administered to 12 patients with chronic obstructive lung disease in order to determine, whether an analeptic action on respiration, which had been found by others in animal studies and in healthy subjects, can also be demonstrated in patients with COLD. Time ventilation showed no statistically significant change. Respiratory rate was increased for a short time, alveolar ventilation showed a slight but significant increase 35 minutes after i.v. injection of fominoben, however no significant change in the first 10 minutes after injection.--Arterial pO2 was slightly but not significantly increased in the first 10 minutes after fominoben, while the same patients showed a significant decrease of pO2 after injection of placebo. As alveolar ventilation at this time had not significantly changed, the increase in pO2 can only be explained by an improvement of regional ventilation-perfusion ratio by fominoben. -In conclusion it can be stated, that a marked stimulative action on respiration by fominoben could not be demonstrated. There was, however, no depression of respiration as it is associated with most other caugh medications. As the drug has been shown to be an excellent caugh sedative, lack of respiratory depression can be considered as a considerable advantage.
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PMID:[Effect of fominoben on ventilation, oxygen uptake and blood gases in patients with obstructive ventilation disorders]. 1 14

Arterial blood gases were not significantly altered by 0.15 mg/kg intravenous dose of diazepam in patients with chronic obstructive lung disease. The PalphaO-2 was significantly reduced and the P-alphaCO-2 increased after administration of 1.5 mg/kg meperidine intravenously and the combination of 1.5 mg/kg meperidine with 0.15 mg/kg diazepam. Diazepam did not, however, significantly increase the ventilatory depression induced by meperidine. Therefore, 0.15 mg/kg diazepam intravenously causes no ventilatory depression by meperidine in patients with chronic obstructive lung diseases.
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PMID:Diazepam and meperidine on arterial blood gases in patients with chronic obstructive pulmonary disease. 23 17

In a 66-year-old patient with chronic obstructive pulmonary disease (COPD) complicated by arterial hypoxemia and repeated episodes of respiratory and right ventricular failure, a satisfactory level of oxygenation could not be maintained despite controlled oxygen therapy. To enable oxygen to be administered without depression ventilation, artificial respiration by means of phrenic nerve stimulation (diaphragm pacing) has been employed. Evidence of clinical improvement since pacing was begun 32 months ago include fewer episodes of respiratory failure and better control of congestive heart failure despite a gradual worsening of pulmonary function.
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PMID:Diaphragm pacing. Application to a patient with chronic obstructive pulmonary disease. 30 48

In seven of 30 ambulatory asthmatics the inhalation of 10% acetylcysteine reduced the FEV1 by more than 10% (range: 14% to 53%). Inclusion of isoproterenol (0.05%) reversed this depression over the entire trial in six of these subjects, while the seventh responded similarly except for the last measurement. It is concluded that the addition of isoproterenol to an acetylcysteine aerosol in the above ratio can eliminate the ventilatory impairment induced by the latter and is therefore indicated for those patients with chronic obstructive lung disease who benefit from a mucolytic agent.
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PMID:Controlled trial of bronchodilator-mucolytic aerosols, combined and separate. 34 59

During the last four years we have used a new cardioselective beta-adrenergic blocking substance, ICI 66.082 (atenolol or Tenormin), alone or in combination with other drugs for treatment of hypertension in a total of 104 patients, including 15 with a chronic obstructive lung disease. Fifty-one patients started treatment with atenolol because of side-effects--especially from the central nervous system--during previous treatment with non-selective beta-blockers, mostly propranolol (Inderal). Mean duration of treatment was 16 months (range 8--36) and mean dosage 163 mg/day. In 18 patients treatment with Tenormin was withdrawn, but only in 10 of them could this be referred to side-effects. Of the 51 patients who complained of or showed side-effects from another beta-blocker, 80% were improved after changing to Tenormin. Of the patients with side-effects from the central nervous system, 73% improved, especially those who complained of nightmares, hallucinations, insomnia or mild depression.
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PMID:Long-term clinical experience with atenolol--a new selective beta-1-blocker with few side-effects from the central nervous system. 36 88

The effect of metoprolol on pulmonary function was compared with that of propranolol and placebo in twelve patients with chronic obstructive lung disease. Propranolol caused a significant reduction in FEV1 compared with metoprolol and placebo. Metoprolol gave a slight reduction compared with placebo. FVC was not significantly influenced by metoprolol, but propranolol caused a significant depression compared both with metoprolol and placebo. The isoprenaline-mediated increase in FEV1 and FVC was not significantly altered after metoprolol compared with placebo. After propranolol the isoprenaline-mediated increases in FEV1 and FVC were 40 and 24% lower respectively than after metoprolol and placebo. Unwanted effects and pulmonary symptoms were at an acceptable level in all cases except in two patients who had to be given i.v. theophyllamine therapy during propranolol treatment. It is concluded that metoprolol exhibits a selective beta1-blocking action and thus may be given to patients with chronic obstructive lung disease provided that adequate beta2-stimulator treatment is given concomitantly.
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PMID:Effects of muliple doses of metoprolol and propranolol on ventilatory function in patients with chronic obstructive lung disease. 79 May 61

Physicians and paramedical personnel often find the early diagnosis and differentiation of obstructive airway diseases to be a challenging problem. The history and physical examination are often not enough to allow the physician to detect either the presence of, or determine the type of, disease present. Patterns of pulmonary function abnormality to determine the presence of obstructive or restrictive defects are discussed. Guidelines useful in the differentiation of obstructive airway diseases are presented. Once a patient with COAD is assessed, the physician needs to outline a therapeutic program after establishing goals with the patient. These goals include (1) improved ability for the patient to achieve relief from symptoms and (2) improved capacity to carry out the activities of daily living. The therapeutic modalities available for the comprehensive care of patients with COAD are discussed. These include general factors such as patient and family education, avoidance of smoking and other inhaled irritants, avoidance of infection, a minimum stress environment, high fluid intake, and proper nutrition. The appropriate use of the medications most commonly employed in the teatment of these patients, eg, bronchodilators, expectorants, antimicrobials, corticosteroids, cromolyn, digitalis, and diuretics, are individually discussed. The use of such respiratory therapy techniques as aerosol therapy, intermittent positive pressure breathing, and oxygen therapy are considered. Application of the specialty of rehabilitation medicine to patients with obstructive airway disease is described. This includes physical therapy with breathing retraining, clapping and postural drainage, and exercise reconditioning, occupational therapy with attention to energy conservation in activities of daily living, psychological considerations, and vocational rehabilitation. Definite benefits that can be demonstrated if the physician employs this type of systematic respiratory care program include a decrease in the frequency and duration of hospital admissions, socioeconomic gains from reduced hospitalizations, a reduction in anxiety, depression and somatic concern, the return of patients to positions of employment and the establishment of a better quality of life. Persistence in making sure the patient continues in a systematic program, including both pharmacological and nonpharmacological modalities, may be the means of assuring maintenance or even improvement in his health. The day-to-day treatment for the majority of patients should remain in the hands of the primary physician. However, community resources must be established to allow the primary physician to provide these patients with adequate comprehensive respiratory care. Development of three levels of care (the primary physician, community respiratory rehabilitation units, and the regional respiratory center) should make superior respiratory care available to every patient with obstructive airway disease.
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PMID:Chronic obstructive airway diseases. Current concepts in diagnosis and comprehensive care. 80 50

Once a diagnosis of COPD is suspected, history, physical examination, pulmonary function tests, chest roentgenogram, sputum analysis, and so forth, are useful to assess the severity of obstructive airways diseases. A comprehensive program of care is then outlined (Table 2). General measures include avoidance of infection and inhalants, humidification, and proper rest and diet. Appropriate medications may include bronchodilators, antibiotics, corticosteroids, cromolyn sodium, digitalis, and diuretics. Inhalation therapy as aerosols, IPPB, and supplemental oxygen may be indicated. Physical therapy with postural drainage, exercise reconditioning, and occupational therapy deserve attention. The day-to-day care of the vast majority of patients with COPD is managed by primary care physicians. This systematic approach to pulmonary rehabilitation will yield definite rewards. Patients will feel and perform better. They will note an improved exercise tolerance, leading to increased activities of daily living. They will experience reduction in the frequency and duration of hospitalization as well as a decrease in anxiety and depression with an improved quality of life.
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PMID:Comprehensive care in chronic obstructive pulmonary disease. 82 54

A well-demarcated U or V-shaped gas density superimposed over the trachea on posteroanterior chest radiographs is due to air in the suprasternal fossa. This is the depression on the skin surface of the neck between the sternal heads of the sternocleidomastoid muscles. The fossa is frequently visualized radiographically in cachectic or very thin people, and in patients with prior laryngectomies. It is also seen in patients with chronic obstructive lung disease and in patients in acute respiratory distress. Because of its typical location and configuration, it should not be confused with an air-fluid level in the esophagus or an upper airway diverticulum.
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PMID:The suprasternal fossa. 83 64

Indirect measures of left ventricular function were studied in seven patients with respiratory failure secondary to chronic obstructive pulmonary disease to determine if there were a relationship between left ventricular function and treatment of the pulmonary disease. All patients were studied during acute episodes while in respiratory failure having arterial Pco2 (Paco2) values greater than 49 torr with no clinical evidence of left ventricular failure. Indirect methods to evaluate left ventricular function included the use of the Swan-Ganz catheter for pulmonary capillary wedge pressure measurement, systolic time intervals, and cardiac output. There was improvement in left ventricular function with treatment of the respiratory failure manifested by decreases in the wedge pressure and pre-ejection period/left ventricular ejection time ratio, and an increase in the dp/dt/pulmonary capillary wedge pressure with treatment of the chronic obstructive pulmonary disease. The improvement in left ventricular function suggests that there is a depression of left ventricular function in respiratory failure. The depressed function improved with therapy of the lung disease without additional medication directed at cardiac function.
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PMID:Left ventricular function during respiratory failure. 87 4


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