Effects of airway tone and volume history on maximal expiratory flow in asthma

Pichurko, Bohdan; Ingram, R. H.

doi:10.1152/jappl.1987.62.3.1133

Cited by 43 publications

(33 citation statements)

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“…At least three possible answers are presented in the literature. The first is provided by BURNS et al [17], PICHURKO et al [39], LIM and co-workers [40,41] and PLISS et al [42], which is based on the concept of relative hysteresis of airway versus lung and first developed by FROEB and MEAD [43]. They found, as did FISH et al [16], that in asthmatics, not only did deep inspiration fail to reverse spontaneous obstruction, it sometimes resulted in worsening of airway narrowing.…”

Section: Evidence Of Asm Involvement In Asthmamentioning

confidence: 99%

“…One important factor determining the magnitude of airway hysteresis is ASM tone and the response of that tone to the stretch induced by deep inspiration; this will be discussed later in the current study. Therefore, the analysis of BURNS et al [17], PICHURKO et al [39], LIM and co-workers [40,41] and PLISS et al [42] highlights the importance of ASM in mediating the deep inspiration-induced changes in airway calibre.…”

Section: Evidence Of Asm Involvement In Asthmamentioning

confidence: 99%

“…The second possible answer takes a complementary view to that of the first [17,39,[40][41][42] and is based on a distinctly different mechanism [22,23,[45][46][47][48][49][50][51]. Both GUNST and co-workers [22,23] and FREDBERG et al [52] focused not so much on the parenchyma and changes of parenchymal hysteresis, but rather called attention to the changes in ASM itself.…”

Section: Evidence Of Asm Involvement In Asthmamentioning

confidence: 99%

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Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

An¹,

Bai²,

Bates³

et al. 2007

European Respiratory Journal

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341

298

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Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma.As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is not certain whether, in asthma, there is a change in the intrinsic properties of ASM, a change in the structure and mechanical properties of the noncontractile components of the airway wall, or a change in the interdependence of the airway wall with the surrounding lung parenchyma. All these potential changes could result from acute or chronic airway inflammation and associated tissue repair and remodelling.Anti-inflammatory therapy, however, does not ''cure'' asthma, and airway hyperresponsiveness can persist in asthmatics, even in the absence of airway inflammation. This is perhaps because the therapy does not directly address a fundamental abnormality of asthma, that of exaggerated airway narrowing due to excessive shortening of ASM.In the present study, a central role for airway smooth muscle in the pathogenesis of airway hyperresponsiveness in asthma is explored.

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Section: Evidence Of Asm Involvement In Asthmamentioning

confidence: 99%

Section: Evidence Of Asm Involvement In Asthmamentioning

confidence: 99%

Section: Evidence Of Asm Involvement In Asthmamentioning

confidence: 99%

See 1 more Smart Citation

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

An¹,

Bai²,

Bates³

et al. 2007

European Respiratory Journal

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341

298

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“…When airway obstruction was induced by hyperventilation with cold air [53], methacholine [41] or histamine [54], a deep inhalation most often resulted in lessening of obstruction that is transient (bronchodilation). The degree of improvement was proportional to the degree of induced obstruction.…”

Section: Human Studiesmentioning

confidence: 99%

The distal airways: are they important in asthma?

Kraft¹

1999

Eur Respir J

131

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Although the airways of <2 mm in diameter have been dubbed the "quiet zone", they do not appear to be so in asthma. Physiological and pathological evidence suggests that the small airways and lung parenchyma participate in asthma pathogenesis, and may explain many of the clinical observations noted.This review presents this evidence, beginning with physiological evidence, followed by pathology and last by imaging studies that evaluate the distal lung. Seminal physiological studies date back to the 1960s, with significant progress in the area of airway smooth muscle and its contribution to airways responsiveness noted over the last several years.The use of bronchoscopy in clinical studies has complemented the autopsy studies in advancing knowledge about airway structural changes appreciated in asthma in the small airways and lung parenchyma. These pathological studies have allowed validation of the physiological, and more recently the imaging studies performed to evaluate this compartment of the lung in asthma.Thus, the evidence suggests that the small airways and parenchyma contribute significantly to asthma pathogenesis. The challenge now lies in evaluating this compartment in the context of its value as a therapeutic target in asthma. Eur Respir J 1999; 14: 1403±1417. Data from the last three decades have suggested that the distal lung, which includes the airways of <2 mm and the lung parenchyma, contributes to asthma pathogenesis. Due to the challenges raised in evaluating this part of the lung, this region has not been studied in the same level of detail as have the larger airways. However, a significant amount of pathological data from autopsy specimens and recently from chronic, stable asthmatics, evaluating the small airways and lung parenchyma, are available. These data, combined with physiological data, support a significant role for the distal lung as a contributor to airway inflammation and hyperresponsiveness. The following review will present this evidence and explore the clinically important issue of the distal lung as a therapeutic target in asthma. Physiology of the distal airways Animal and in vitro studiesThe small airways of <2 mm in diameter are pathways of low resistance, and normally contribute~10% of the total resistance to flow. These observations were made in, seminal contributions by MACKLEM and MEAD [1, 2] using a retrograde catheter technique. Using excised dog lobes, they placed a catheter containing bell shaped polyethylene tubing at one end. The bell was wedged into a bronchus with the catheter extending peripherally through the parenchyma and pleura. They showed that the peripheral resistance (Rp) was too small to detect at >80% of vital capacity (VC), but increased at lower volumes to 15% of the total lung resistance at 1% of VC. These data are in keeping with WEIBEL [3], who demonstrated that the cross-sectional area of the small airways was significantly larger than that of the central airways. BROWN et al. [4] further evaluated the effects of small airways occlusion...

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“…At variance to this, quite consistently [23,24], M/P ratios increase during induced constriction. The mechanical basis for a constrictor effect of DI can be explained by disparities between the hysteresis of airways and parenchyma as proposed by FROEB and MEAD [25].…”

Section: Discussionmentioning

confidence: 74%

Reduction in bronchodilation following a deep inhalation is poorly related to airway inflammation in asthma

Pacini

Filippelli²,

Duranti³

et al. 1999

Eur Respir J

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In patients with bronchial asthma, forced expiratory flows are differently sensitive to a previous volume history. A reduced ability of a deep inhalation (DI) to dilate obstructed airways has been hypothesized to be a physiological marker for the degree of airway responsiveness and to relate to the presence and magnitude of inflammation in the lung, even in mild stable asthma. However, there are at present doubts as to whether functional changes could be used as a substitute for airway inflammation studies.In order to investigate the interrelations among airway inflammation, bronchial hyperresponsiveness and effects of volume history, 58 consecutive asthmatics with mild to moderate asthma were studied. The effects of DI were assessed as the isovolumic ratio of flows from forced expiratory manoeuvres started from maximal (M) or partial (P) lung inflation. Airway inflammation was assessed by using induced sputum. Sputum was analysed for total and differential cell counts, and levels of eosinophil cationic protein (ECP) which reflects eosinophil activation. Airway responsiveness was assessed as the provocative concentration of histamine which caused a 20% fall in forced expiratory volume in one second (FEV1) from control (PC20).The M/P ratio was significantly related to ECP (r=-0.31, p<0.03) and eosinophils (r=-0.29, p<0.03), FEV1/vital capacity (VC) (r=0.32; p<0.01), clinical score (r=-0.33; p<0.03) and age (r=-0.41; p<0.0001). In a stepwise multiple regression analysis including age, score, baseline lung function, ECP, number of eosinophils and the response to b 2 -agonist, age (p<0.037) predicted a small amount of the variance in M/P ratio (r 2 =0.12). It is concluded that volume history response is substantially independent of both sputum outcomes (inflammatory cell number and eosinophil cationic protein) and bronchial hyperresponsiveness; rather it seems to be associated with anthropometric characteristics. Functional aspects do not provide information on eosinophilic, probably central, airway inflammation. Eur Respir J 1999; 14: 1055±1060. In patients with bronchial asthma maximal expiratory flow is affected by a deep inhalation (DI) varying from an increase, to no effect, to a decrease in expiratory flow. These changes relate to the site and mechanism of the obstructive process [1]. A reduction in bronchodilation following a DI has been shown to be positively related to the severity of airway inflammation [2]. An increase in the bronchodilator effect of a DI, after corticosteroid administration, has consistently been reported [2±4]. Furthermore, the bronchodilator effect of DI is inversely related to the degree of responsiveness to a subsequent methacholine challenge in mild asthma [5]. Thus, several lines of evidence suggest that the blunting of the dilator effect of DI during obstruction could serve as a physiological marker for the degree of airway responsiveness and may relate to the presence and magnitude of inflammation in the lung even in mild stable asthma [2].This hypothesis is based eithe...

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Effects of airway tone and volume history on maximal expiratory flow in asthma

Cited by 43 publications

References 0 publications

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

The distal airways: are they important in asthma?

Reduction in bronchodilation following a deep inhalation is poorly related to airway inflammation in asthma

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