Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used a wedged bronchoscope technique in conjunction with an in situ isolated perfused left lower lobe preparation in anesthetized dogs to examine cold-associated airway modulation of peripheral lung responses to dry airflow, hypocapnia, and aerosols of histamine and hypertonic NaCl. In this preparation, airway wall temperature was rapidly lowered by decreasing the temperature of blood perfusing the wedged sublobar segment. Cooling significantly attenuated responses to dry air, hypertonic NaCl aerosol, and hypocapnic challenge. In contrast, cooling did not affect peripheral lung responses to aerosolized histamine. Thus, cooling per se does not inhibit the responsiveness of smooth muscle. We conclude that, depending on the stimulus, cooling can modulate airway reactivity. We speculate that cooling attenuates hypocapnia, hypertonic aerosol, and dry air-induced bronchospasm via a cold induced reduction in neuronal activity or mediator production and release.
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PMID:Airway cooling: stimulus specific modulation of airway responsiveness in the canine lung periphery. 193 28

We report the case of an 82-year old male patient without history of chronic obstructive lung disease in whom a sudden respiratory distress syndrome with sibilant rales in both lungs revealed a moderately severe pulmonary embolism, later confirmed by angiography. Bronchospasm occurring in the acute phase of pulmonary embolism may be expressed as acute asthma refractory to bronchodilators. This bronchoconstriction, seldom detectable clinically, seems to be related to regional alveolar hypocapnia in the territories embolized and to platelet-produced mediators, through a vagus nerve-mediated reflex. It must not hide pulmonary embolism, particularly in a suggestive context and when bronchodilators are ineffective.
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PMID:[Bronchospasm disclosing pulmonary embolism]. 207 66

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

The purpose of this study was to investigate the pulmonary effects of hyperventilation in anesthetized, mechanically ventilated guinea pigs. Airway resistance (Raw), dynamic lung compliance (CDyn), blood pressure (BP), heart rate (HR), arterial blood gases (PaO2, PaCO2), pH and arterial plasma HCO3- were measured before and after a 10-min period of hyperventilation produced by increasing the respiratory rate from 60 to 120 breaths/min while maintaining tidal volume at 4 ml. There was a significant increase in Raw and decrease in CDyn lasting up to 20 min after hyperventilation was stopped with no change in BP and HR. PaO2 was reduced from 109 +/- 3 mm Hg before to 53 +/- 7 mm Hg at 5 min after hyperventilation. The Raw and CDyn changes were prevented and reversed with the bronchodilators salbutamol and aminophylline indicating that reversible bronchospasms are induced in guinea pigs following a period of hyperventilation. Additional studies demonstrated that the pulmonary mechanical responses to hyperventilation were not changed by vagotomy, ventilation with high CO2 or by pretreatment with chlorpheniramine, methysergide, atropine, indomethacin, FPL 55712 or calcium-influx blockers. These results indicate that neither vagal reflexes, airway hypocapnia, receptors of histamine, serotonin, acetylcholine nor the products of arachidonic acid metabolism were involved in hyperventilation-induced bronchospasm in guinea pigs.
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PMID:Hyperventilation-induced bronchoconstriction in guinea pigs. 393 Apr 9

Mechanical ventilation can worsen morbidity and mortality by causing ventilator-associated lung injury, especially where adverse ventilatory strategies are employed. Adverse strategies commonly involve hyperventilation, which frequently results in hypocapnia. Although hypocapnia is associated with significant lung alterations (e.g., bronchospasm, airway edema), the effects on alveolar-capillary permeability are unknown. We investigated whether hypocapnia could cause lung injury independent of altering ventilatory strategy. We hypothesized that hypocapnia would cause lung injury during prolonged ventilation, and would worsen injury following ischemia-reperfusion. We utilized the isolated buffer-perfused rabbit lung model. Pilot studies assessed a range of levels of hypocapnic alkalosis. Experimental preparations were randomized to control groups (FI(CO(2)) = 0.06) or groups with hypocapnia (FI(CO(2)) = 0.01). Following prolonged ventilation, pulmonary artery pressure, airway pressure, and lung weight were unchanged in the control group but were elevated in the group with hypocapnia; elevation in microvascular permeability was greater in the hypocapnia versus control groups. Injury following ischemia-reperfusion was significantly worse in the hypocapnia versus control groups. In a preliminary series, degree of lung injury was proportional to the degree of hypocapnic alkalosis. We conclude that in the current model (1) hypocapnic alkalosis is directly injurious to the lung and (2) hypocapnic alkalosis potentiates ischemia-reperfusion-induced acute lung injury.
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PMID:Injurious effects of hypocapnic alkalosis in the isolated lung. 1093 60

Bronchial asthma is a chronic inflammatory disorder of the airways in which many cells play a role, in particular mast cells, eosinophils, neutrophils, T-lymphocytes and epithelial cells. In susceptible individuals this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and/or in the early morning. These symptoms are usually associated with variable and extensive limitations of airflow in the bronchi reversible spontaneously or by treatment. It has been shown that restrain of the effectors of stress response participate in the pathogenesis of bronchial asthma. Anger that is not expressed and frustrations may activate the limbic stress pathway. Thus, the released neurotransmitters followed by excitation thus causing psychogenic (mental or emotional) stress. It is also known that emotional stress may be responsible for the exacerbation of asthma. Namely, pronounced emotions cause hyperventilation and hypocapnia inducing bronchospasm. Certain psychological personality features are related to adaptive or inadequate body response to numerous life events. Thus, until the beginning of the last century, bronchial asthma was referred to as asthma nervosa, because clinicians clearly observed the psychological profile of patients with predominant fear of asphyxia and recurrent attacks of paroxysmal dyspnoea. Besides, increased sensitivity, repression of aggressive feelings and expressive empathy have been identified as the most frequent psychological characteristics of asthmatic patients. However, scientists are still far from a full understanding of bronchial asthma pathogenesis. The contribution of psychic factors has become meaningful in the understanding of the development of bronchial asthma. Having in mind that in the majority of patients asthma is a lifelong condition, there is a hope that further investigations of bronchial asthma psychogenesis will improve prevention and treatment of this disease.
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PMID:[The role of psychic factors in the pathogenesis of bronchial asthma]. 2162 67