Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Airway mucociliary dysfunction leading to a depression of mucus transport has been demonstrated in patients with acute and chronic bronchitis, cystic fibrosis, and bronchial asthma; use of bronchodilators that might further impair mucociliary function, therefore, generally has been discouraged. Atropine and ipratropium bromide are cholinergic antagonists that are effective bronchodilators in various clinical settings. Atropine has been shown to block the production of respiratory secretions in response to cholinergic stimulation, but to have no effect on baseline secretions. Atropine has also been clearly demonstrated to depress ciliary beat frequency and to slow airway mucociliary clearance, whereas the short-term and long-term administration of ipratropium bromide at higher than clinically recommended doses seems to lack these effects. No satisfactory explanation has thus far been offered for this difference between the two cholinergic antagonists. Nevertheless, with respect to airway mucociliary function, ipratropium bromide appears to be preferable to atropine in the treatment of obstructive airways disease.
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PMID:Effect of ipratropium bromide on airway mucociliary function. 294 58

Bronchodilators (xanthines, adrenergics, and parasympatholytics) have been used for years in the treatment of airway obstruction associated with cystic fibrosis. Their effectiveness in bringing about consistent and significant reversal of airway obstruction remains a topic for debate. A review of the literature suggests that the majority of patients with cystic fibrosis have hyperresponsive and hyperactive airways and will respond favorably to bronchodilators, at least some of the time. Bronchial hyperresponsiveness tends to be greater in patients with advanced disease than in mildly affected ones. Responses to bronchodilators appear to be greatest when airway disease is mild-to-moderate, when there is a documented excessive bronchial hyperresponsiveness to nonspecific bronchoconstrictors (methacholine, histamine), and when the patients are young. The response to intravenous xanthine and terbutaline is best when patients experience an acute pulmonary exacerbation and when aerosolized bronchodilators are relatively ineffective. Patients with advanced airway destruction and obstruction have a high degree of airway wall instability, which may be worsened by inhaled bronchodilators. Adrenergic and parasympatholytic aerosols are equally effective; combining them in optimal doses may be more beneficial than using either alone. Atropine and ipratropium bromide may be more effective in adults than children, but this remains to be further evaluated. Some of the apparently poor responses to inhaled bronchodilators are likely due to inadequate dosing. In conclusion, most patients with cystic fibrosis are likely to benefit from bronchodilator therapy when given in adequate doses, appropriate combinations, and by the appropriate route.
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PMID:Effectiveness of bronchodilators in cystic fibrosis. 861 Jul 13

To test the hypothesis that cutaneous active vasodilation in heat stress is mediated by a redundant cholinergic cotransmitter system, we examined the effects of atropine on skin blood flow (SkBF) increases during heat stress in persons with (CF) and without cystic fibrosis (non-CF). Vasoactive intestinal peptide (VIP) has been implicated as a mediator of cutaneous vasodilation in heat stress. VIP-containing cutaneous neurons are sparse in CF, yet SkBF increases during heat stress are normal. In CF, augmented ACh release or muscarinic receptor sensitivity could compensate for decreased VIP; if so, active vasodilation would be attenuated by atropine in CF relative to non-CF. Atropine was administered into skin by iontophoresis in seven CF and seven matched non-CF subjects. SkBF was monitored by laser-Doppler flowmetry (LDF) at atropine treated and untreated sites. Blood pressure [mean arterial pressure (MAP)] was monitored (Finapres), and cutaneous vascular conductance was calculated (CVC = LDF/MAP). The protocol began with a normothermic period followed by a 3-min cold stress and 30-45 min of heat stress. Finally, LDF sites were warmed to 42 degrees C to effect maximal vasodilation. CVC was normalized to its site-specific maximum. During heat stress, CVC increased in both CF and non-CF (P < 0.01). CVC increases were attenuated by atropine in both groups (P < 0.01); however, the responses did not differ between groups (P = 0.99). We conclude that in CF there is not greater dependence on redundant cholinergic mechanisms for cutaneous active vasodilation than in non-CF.
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PMID:Cholinergic mechanisms of cutaneous active vasodilation during heat stress in cystic fibrosis. 1760 Jan 58