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The contractile lability of smooth muscle in asthmatic airway hyperresponsiveness

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References

  • Papers of special note have been highlighted as:
  • * of interest
  • ** of significant interest
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*  In that review, a table is presented to summarize the studies published before 2012 in which the contractile capacity of airway smooth muscle between asthmatics and non-asthmatics has been investigated. Overall, no consistent trend was reported in between studies, although differences in either direction were described.

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**  This study confirmed prior studies showing that the contractile capacity of airway smooth muscle derived from both the trachea and the bronchi is not different between asthmatics and non-asthmatics. Ultimately, it indicates that if hypercontractility of airway smooth muscle is consistently present in asthma, it has to be a transient feature that is acquired in vivo due to other alterations.

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*  This study demonstrated that ventilation heterogeneity in asthmatic patients is an independent predictor of the degree of airway responsiveness to methacholine before and after treatment with a corticosteroid.

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*  This study demonstrated that affecting mucosal blood flow by vasoactive substances in the airways of guinea pigs in vivo alters the degree of airway responsiveness by regulating the clearance of the spasmogen used to trigger airway smooth muscle contraction.

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*  This study demonstrated that fibrin, a plasmatic protein that leaks into the airways during inflammation, increases airway responsiveness by altering the surfactant and, concomitantly, the surface tension.

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*  This study demonstrated that the enhanced narrowing of excised airway segments derived from patients with an history of asthma is due to an increased mass of airway smooth muscle, and that the magnitude of bronchodilation in response to simulated deep inspiration is identical between asthmatic and non-asthmatic airways.

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*  This study demonstrated that mere exposure to tone elicited by repetitive deliveries of a spasmogen enhances airway responsiveness in vivo in mice by increasing the contractile capacity of airway smooth muscle.

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