Observations on the physiological interactions between obesity and asthma

Observations on the physiological interactions between obesity and asthma
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DOI:
10.1152/japplphysiol.01260.2007
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发表时间:
2008-11-01
影响因子:
3.3
通讯作者:
McFadden, E. R., Jr.
McFadden, E. R., Jr.
中科院分区:
医学2区
文献类型:
--
作者:
Nicolacakis, Katina;Skowronski, Mary E.;McFadden, E. R., Jr.

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Nicolacakis K、Skowronski ME、Coreno AJ、West E、Nader NZ、Smith RL、McFadden ER Jr. 肥胖与哮喘之间生理相互作用的观察。 J Appl Physiol 105: 1533-1541, 2008。首次发表于 2008 年 9 月 11 日; doi:10.1152/japplphyol.01260.2007.-为了探讨哮喘和肥胖是否具有重叠的致病特征,我们检查了每种疾病单独和联合对肺功能多个方面的影响。我们推断,如果它们通过类似的机制影响肺部,那么共病状态下的个体生理表现应该以复杂的方式相互作用。如果不是,那么异常应该简单地添加。我们使用标准技术测量了 52 名正常患者、53 名哮喘患者、52 名肥胖患者以及 53 名哮喘和肥胖患者的比电导、肺量测定、肺容量和气道对肾上腺素能和胆碱能激动剂的反应性。每组的子集进行六分钟的步行。哮喘显着降低了比电导和肺活量变量,同时增加了气道反应性和残气量。肥胖还降低了肺活量变量以及肺总容量和功能残气量。残余气量、比电导和气道反应性未改变。随着合并症的发生,疾病特异性的紊乱会以代数方式增加。孤立存在的特征在组合中似乎没有变化,而共享特征则根据各个方向的变化而增加或减少。没有观察到协同相互作用。体重指数与哮喘患者的肺活量和肺容量相关性较弱,但与电导率或支气管反应性无关。运动表现对分化没有帮助。我们的研究结果表明哮喘和肥胖似乎通过不同的过程影响呼吸系统。
Nicolacakis K, Skowronski ME, Coreno AJ, West E, Nader NZ, Smith RL, McFadden ER Jr. Observations on the physiological interactions between obesity and asthma. J Appl Physiol 105: 1533-1541, 2008. First published September 11, 2008; doi:10.1152/japplphysiol.01260.2007.-To explore whether asthma and obesity share overlapping pathogenic features, we examined the impact of each alone, and in combination, on multiple aspects of lung function. We reasoned that if they influenced the lungs through similar mechanisms, the individual physiological manifestations in the comorbid state should interact in a complex fashion. If not, then the abnormalities should simply add. We measured specific conductance, spirometry, lung volumes, and airway responsiveness to adrenergic and cholinergic agonists in 52 normal, 53 asthmatic, 52 obese, and 53 asthmatic and obese patients using standard techniques. Six-minute walks were performed in subsets from each group. Asthma significantly lowered specific conductance and the spirometric variables while increasing airway reactivity and residual volume. Obesity also reduced the spirometric variables as well as total lung capacity and functional residual capacity. Residual volume, specific conductance, and airway responsivity were unaltered. With comorbidity, the disease-specific derangements added algebraically. Features that existed in isolation appeared unchanged in the combination, whereas shared ones either added or subtracted depending on the individual directional changes. Synergistic interactions were not observed. Body mass index weakly correlated with spirometry and lung volumes in asthma, but not with specific conductance or bronchial reactivity. Exercise performance did not aid in differentiation. Our findings indicate asthma and obesity appear to influence the respiratory system through different processes.