Source:http://linkedlifedata.com/resource/pubmed/id/14766781
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2004-4-12
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pubmed:abstractText |
Measures of airway resistance (Raw) during deep inspiration (DI) suggest that asthmatic subjects possess stiffer, more reactive airway smooth muscle. There is evidence that one can enhance airway reactivity in healthy lungs by prohibiting DI for an extended period. The present study had two goals. First, we determined whether the maximum dilation capacity of asthmatic subjects depended on the rate of the DI. Second, we investigated whether the enhanced reactivity in healthy humans might derive from additional mechanisms not present in asthmatic subjects. For the first goal, we tracked Raw in seven healthy and seven asthmatic subjects during a noncoached DI, a DI with a 5- to 10-s breath hold at total lung capacity, and a rapid DI. We found that the minimum resistance achieved at total lung capacity was independent of the manner in which the DI was performed. For the second goal, we tracked the rate of return of Raw after a DI as well as dynamic lung elastance before and after the DI, at baseline and after bronchial challenge. A drop in lung elastance post-DI would indicate reopening of lung regions and/or reduced heterogeneities. The data show that constricted healthy but not asthmatic subjects produce longer lasting residual dilation. Hence, a portion of the enhanced reactivity in a healthy subject's response to prohibition of DIs is likely due to airway closure and/or atelectasis that can be ablated with a DI. We conclude that preventing DIs does not ensure that healthy subjects will transition entirely to an asthmatic-like hyperreactive lung state.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
8750-7587
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
96
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1808-14
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:14766781-Adult,
pubmed-meshheading:14766781-Airway Resistance,
pubmed-meshheading:14766781-Asthma,
pubmed-meshheading:14766781-Bronchi,
pubmed-meshheading:14766781-Bronchoconstriction,
pubmed-meshheading:14766781-Bronchoconstrictor Agents,
pubmed-meshheading:14766781-Case-Control Studies,
pubmed-meshheading:14766781-Female,
pubmed-meshheading:14766781-Humans,
pubmed-meshheading:14766781-Inhalation,
pubmed-meshheading:14766781-Lung Compliance,
pubmed-meshheading:14766781-Male,
pubmed-meshheading:14766781-Methacholine Chloride,
pubmed-meshheading:14766781-Respiratory Mechanics,
pubmed-meshheading:14766781-Total Lung Capacity
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pubmed:year |
2004
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pubmed:articleTitle |
Relating maximum airway dilation and subsequent reconstriction to reactivity in human lungs.
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pubmed:affiliation |
Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA. klutch@bu.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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