Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1-(2-Methoxy-2-phenyl)-ethyl-4-(2-hydroxy-3-methoxy-3-phenyl)-propyl-iperazine-dihydrochloride (zipeprol, Respilene) is a substance of non-phenanthrenic chemical structure. In the cat, it antagonised cough induced by stimulation of the superior laryngeal nerve or by direct mechanical excitation of the sensitive tracheo-bronchial receptors. The efficacy of zipeprol after enteral administration made it possible both to establish good intestinal absorption and to rank it favourably in relation to several major antitussive reference products; codeine, codethyline, dextromethorphan, diphenhydramine and pentoxyverine. The activity of zipeprol was superior or equal to that of all these substances, excdept codeine. The antitussive properties appeared to be due to a central action. Other properties have been demonstrated which suggest at least a supplementary mechanism in the inhibition of cough, in addition to the central action. These consisted of slight antihistamine and anticholinergic properties, marked local-anesthetic potency and bronchospasmolytic activity. This latter property was demonstrated by the inhibition of histamine and serotonin induced bronchospasm in the guinea-pig. In vitro, using human sputum, zipeprol had a mucolytic action, shown by a decrease in sputum vis viscosity and lysis of DNA and AMPS fibrils. In the dog, at high doses, zipeprol unlike codeine, did not inhibit central stimulation of respiration by hypercapnia, in addition no modification of ventilatory dynamics or blood gases was seen. On the basis of these results, zipeprol can be considered as possessing no respiratory depressant effect even in the upper ranges of its antitussive doses.
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PMID:General pharmacological properties of a new non-opiate antitussive: zipeprol (3024 CERM). I. Action on respiratory function and acute toxicity. 0 57

Elevated plasma antidiuretic hormone (ADH) levels were noted in seven patients with status asthmaticus during the acute illness. These values returned to normal with resolution of the disease. The mechanism of this release is not completely understood but is consistent with the hypothesis that bronchospasm leads to decreased pulmonary blood flow, decreased volume return to the left atrium, and stimulation of the atrial volume receptors regulating ADH release. Planning for fluid therapy in patients with status asthmaticus should take into account a high probability of increased plasma ADH concentration during the acute illness. Water intoxication as well as hypoxia and hypercarbia should be considered as a possible cause of an altered state of consciousness associated with status asthmaticus.
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PMID:Elevated plasma antidiuretic hormone levels in status asthmaticus. 124 95

In clinical practice, bronchospasm could be facilitated by hypoxia and by hypercapnia. In this study we assessed the influence of breathing a hypoxic (FIO2 = 0.10) or a hypercapnic (FICO2 = 0.08) gas mixture on the response to nebulized histamine (2% solution for 5 min) in anesthetized, tracheotomized, paralyzed and mechanically ventilated rabbits. Total respiratory resistance (Rrs) and elastance (Ers) were derived by least-square analysis from the relationship between tracheal pressure and flow. Control values of Rrs were larger during hypoxia and hypercapnia than in air while the values of Ers were similar. The absolute change in Rrs after histamine was similar in air and hypoxia, and larger in hypercapnia. The relative change, however, was smaller in hypoxia than in the two other conditions. Ers was also substantially increased by histamine and, contrary to Rrs, remained high 60 min after the aerosol. The results suggest: (1) that both hypoxia and hypercapnia increase airway resistance but do not change tissue properties; (2) that the response to histamine is depressed by hypoxia; (3) that a substantial part of the immediate response, and most, if not all, of the residual response after 60 min is due to changes in lung tissue viscoelastic properties.
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PMID:Changes in inspired gas composition and experimental bronchospasm in the rabbit. 148 Aug 38

This study analyzed the history, clinical characteristics, and acid-base data in relation to the speed of decompensation in 34 patients intubated and mechanically ventilated for severe asthma. Three patterns of decompensation were established according to the delay between the onset of symptoms and endotracheal intubation: Group I, rapid decompensation (less than 3 hours); Group II, gradual development of respiratory failure (9.2 +/- 7.7 days); Group III, acute exacerbation after unstable asthma (4.2 +/- 3.6 days). Patients who developed sudden asphyxia (Group I) showed features distinct from those with a gradual worsening. Sudden asphyxic asthma is more frequent in young men and is characterized by a severe mixed acidosis with extreme hypercapnia (mean PaCO2 = 112.8 +/- 43.9 mm Hg), a higher incidence of respiratory arrest, and silent chest upon admission. Recovery is more rapid, with a shorter duration of mechanical ventilation (33.7 +/- 25.3 h versus 91.4 +/- 64.1 h in Group II). Several arguments suggest that bronchospasm plays the primary role in the pathogenesis of sudden asphyxic asthma.
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PMID:Sudden asphyxic asthma: a distinct entity? 236 57

A previously unrecognized, striking movement disorder has been observed in 10 premature infants with severe bronchopulmonary dysplasia. Chronic hypoxemia, hypercarbia, bronchospasm, and inadequate nutrition were present in all. The movement disorder developed from approximately the third postnatal month. The dominant movements involve the limbs, neck, trunk, and oral-buccal-lingual structures. The limb movements were most prominent distally and consisted of rapid, random, jerky movements (similar to chorea) and "restless" movements (similar to akathisia). Similar movements of the neck and face were observed; tongue movements had a "darting" quality. The oral-buccal-lingual movements were similar to the dyskinesia of older patients. Movements were exacerbated during episodes of respiratory failure and attenuated during sleep. All infants exhibited feeding disorders, largely due to tongue movements. In 3 infants treated with clonazepam, there was striking improvement in motor function, including feeding. The natural history was partial or complete resolution or a static course. Thus, of the 7 surviving infants, the movements were absent (without therapy) at 15, 18, and 30 months of age. In the remaining 4 infants (3 of whom receive clonazepam), the movements, though attenuated, persisted at 6, 12, 15 and 21 months of age, respectively. Neuropathologically, 1 infant showed neuronal loss with astrocytosis in caudate, putamen, globus pallidus, and thalamus. These data defined a previously unrecognized extrapyramidal movement disorder of infants with severe bronchopulmonary dysplasia; pathogenesis may be related to chronic hypoxemia.
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PMID:Movement disorder of premature infants with severe bronchopulmonary dysplasia: a new syndrome. 237 Nov 10

In three consecutive patients suffering from life-threatening asthma in a comatose state (mean age: 37 +/- 4 yr; Glasgow coma score: 3; bilateral mydriasis), intracranial pressure was monitored with an extradural transducer set-up a mean of 2 h after the onset of the coma. The aims were to detect intracranial hypertension and to improve its therapy. Basal therapy associated: 1) mechanical ventilation; 2) theophylline 1.5 g X 24 h-1, salbutamol 30 mg X 24 h-1, hydrocortisone 2 g X 24 h-1, pancuronium 0.5 mg X kg-1 X 24 h-1; 3) pentobarbitone 35 mg X kg-1 X 24 h-1, normal hydration, normothermia and 30 degrees head-up tilt. If the intracranial pressure rose above 15 mmHg, an i.v. bolus of pentobarbitone (5 mg X kg-1) was given if the barbiturate blood level was equal or below 100 micrograms X l-1. In case of failure, a dose of mannitol (20 mg) completed the therapy if blood therapy was equal or below 320 mosm X l-1. All patients developed intracranial hypertension (21, 53 and 23 mmHg, respectively). The intracranial hypertension followed the bronchospasm and disappeared with it. Hypoxaemia, hypercapnia and high peak airway pressures could explain the intracranial hypertension. All patients recovered without sequelae. This data should make us use with great care all treatments likely to increase the intracranial pressure during life-threatening asthma.
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PMID:[Intracranial hypertension during status asthmaticus]. 357 44

Attacks of acute airway obstruction often complicate the course of chronic obstructive pulmonary disease (COPD). In asthmatic subjects, bronchospasm triggers an increase in respiratory drive, which results in hyperventilation and hypocapnia. In the present study, we assessed the effects of acute bronchoconstriction induced by aerosolized methacholine on breathing and lung mechanics in 12 patients with stable COPD. Even low doses of methacholine markedly increased airway resistance and caused hyperinflation and decreased inspiratory muscle performance in the patients. Increasing airway obstruction produced a progressive rise in PCO2 despite an increase in minute ventilation. Breathing frequency and average inspiratory flow were greater, but tidal volume decreased because of shortening of the inspiratory duration. The magnitude of CO2 retention during acute bronchoconstriction was inversely related to the changes in tidal volume and inspiratory time (p less than 0.01 for each). In subjects with COPD, the occlusion pressure response to progressive hypercapnia failed to increase during bronchoconstriction. These results show that patients with COPD retain CO2 during acutely increasing airway obstruction induced by bronchoconstriction partly because of a rapid shallow breathing pattern that reduces alveolar ventilation.
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PMID:The effects of acute bronchoconstriction on respiratory activity in patients with chronic obstructive pulmonary disease. 391 92

Forty children with severe asthma were admitted to an intensive care unit from 1970 to 1981. Criteria of severity were alteration of consciousness, circulatory failure, hypercarbia greater than 7 KPa and paradoxical pulse greater than 35 mmHg persisting in spite of correct treatment. Some therapeutic measures (oxygen, corticosteroids, antibiotics, hydratation) were not modified during this period. On the contrary, bronchodilators, used at a higher dose since June 1980, were very effective on bronchospasm without side effects, making controlled ventilation unnecessary. These results seem to be very encouraging but have to be confirmed.
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PMID:[Therapy of severe asthma crisis in children. Therapeutic course. A propos of 40 cases]. 641 34

A 31-year-old man with legionnaires' disease, who presented with severe pneumonia and hypoxemia, later developed severe bronchospasm and marked hypercapnia, a complication not previously reported in Legionella infection. He responded to therapy with erythromycin and a bronchodilator.
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PMID:Legionnaires' disease. Association with severe bronchospasm and hypoventilation. 710 70

An EEG has been recorded during surgery for a cervico-mediastinal desmoid fibroma in a 3-year-old child. Soon after anesthetic induction a bronchospasm occurred, followed by major respiratory difficulties. During more than 3 h, hypercapnia reaching 15-24 kpa was noted without hypoxia. Meanwhile the EEG recording was inactive. The respiratory difficulties subsided only with the surgical liberation of the trachea. As the hypercapnia decreased, the EEG began to show "burst suppressive" activity. Progressively the tracing was more and more continuous with slow waves until complete recovery. The following day the EEG was quite normal. The mechanisms of these EEG features are discussed with regards to anesthetic drugs and to brain hypercapnic edema.
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PMID:[EEG recordings in prolonged hypercapnia during surgery of a cervico-mediastinal tumor in a 3-year-old child]. 715 43


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