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1 Dipartimento di Medicina Interna, Università di Genova, 16132 Genova; and 2 Fisiopatologia Respiratoria, Azienda Ospedaliera S. Croce e Carle, 12100 Cuneo, Italy
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Deep breaths taken before inhalation of methacholine attenuate the decrease in forced expiratory volume in 1 s and forced vital capacity in healthy but not in asthmatic subjects. We investigated whether this difference also exists by using measurements not preceded by full inflation, i.e., airway conductance, functional residual capacity, as well as flow and residual volume from partial forced expiration. We found that five deep breaths preceding a single dose of methacholine 1) transiently attenuated the decrements in forced expiratory volume in 1 s and forced vital capacity in healthy (n = 8) but not in mild asthmatic (n = 10) subjects and 2) increased the areas under the curve of changes in parameters not preceded by a full inflation over 40 min, during which further deep breaths were prohibited, without significant difference between healthy (n = 6) and mild asthmatic (n = 16) subjects. In conclusion, a series of deep breaths preceding methacholine inhalation significantly enhances bronchoconstrictor response similarly in mild asthmatic and healthy subjects but facilitates bronchodilatation on further full inflation in the latter.
forced expiratory volume in 1 s; specific airway conductance; partial flow-volume curve; functional residual capacity; residual volume
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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RECENT STUDIES HAVE SHOWN that deep breaths taken immediately before inhalation of methacholine (MCh) greatly modulate the bronchoconstrictor response in normal (10, 12, 21) but not in asthmatic (10) subjects. This would suggest that the shortening capacity of airway smooth muscle is reduced by previous lung stretching in healthy subjects, and the lack of such a bronchoprotective mechanism may be responsible for airway hyperresponsiveness in asthma. A mechanistic interpretation of the above studies is, however, limited by the use of forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC), measurements that are highly and variably affected by the full lung inflation preceding the forced expiratory maneuver. During induced bronchoconstriction, a full inflation transiently increases airway caliber, and the magnitude of this increase depends on the relative magnitude of the distending force of lung parenchyma and the constrictor force of airway smooth muscle (17). Therefore, any parameter derived from a full forced expiratory maneuver, including FEV1 and FVC, will depend on both airway smooth muscle shortening capacity and airway wall response to a deep breath.
It is reasonable to postulate that, if the lack of a bronchoprotective effect by multiple deep breaths taken before inhaling a constrictor agent in asthma is due to the inability to reduce the shortening capacity of airway smooth muscle, then the different effects of the deep breaths on airway response to MCh between asthmatic and normal subjects should be equally detected by measurements preceded or not preceded by a full lung inflation. By contrast, a bronchoprotective effect of deep breaths visible only with FEV1 and FVC would suggest a difference in distensibility of the airways in response to a single deep breath between normal and asthmatic subjects rather than in the shortening capacity of airway smooth muscle.
The present paper reports on two sequential studies aimed at addressing this point. In a first study, the effects of a single dose of inhaled MCh, preceded or not by a series of deep breaths, were compared at 1 and 10 min in healthy and mild asthmatic subjects by using measurements of airway caliber either requiring or not requiring full lung inflation. Although a bronchoprotective effect by deep breaths was observed with FEV1 and FVC in the healthy subjects, parameters not preceded by full inflation tended to change more with than without the deep breaths. To better investigate this effect, a second study was conducted by using a protocol without measurements requiring full lung inflation and extending the observation time to 40 min, during which deep breaths were carefully avoided.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
A total of 11 healthy and 26 asthmatic subjects (Table 1) participated in the study after giving informed consent, as approved by the local ethics committee. Asthmatic subjects had mild intermittent disease (16). At the time of the study, they were in stable clinical conditions, with a FEV1 of >70% of predicted (19) without taking inhaled or oral steroids, cromolyn, antihistamine, or regular bronchodilators. Subjects using short-acting
2-agonists
on demand were requested to avoid using them for 12 h before
studies. Before entering the study, each asthmatic subject was tested
for the effects of the deep breaths on airway caliber. To this purpose, specific airway conductance (sGaw) was measured (see below) before and
again 2, 4, and 6 min after five deep breaths (i.e., from tidal
breathing level to full inflation) taken within 30 s through the
mouth without breath holding. Five asthmatic patients with a reduction
of sGaw of >15% of the value recorded before the deep breaths were
not included in the studies.
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Lung Function Measurements
Spirometry and flow-volume curves were obtained by using a mass flowmeter (SensorMedics, Yorba Linda, CA) and numerical integration of the flow signal. Airway resistance was measured by whole body plethysmography (Vmax 6200 Autobox, SensorMedics) while the subject was panting slightly >1.7 Hz. Immediately after each airway resistance measurement, thoracic gas volume (TGV) was measured by panting against a closed shutter at a frequency slightly <1 Hz, and sGaw was calculated as 1/(TGV × airway resistance). Functional residual capacity (FRC) was corrected for the difference between TGV and the end-expiratory volume of the four to six preceding tidal breaths. To obtain partial flow-volume curves superimposed at a constant absolute lung volume, TGV was first measured, and then a complete forced expiration initiated from end-tidal inspiration was performed soon after the reopening of the shutter. In each subject, partial forced expiratory flow (
part) was always measured at the same absolute
lung volume (between 30 and 40% of control FVC), depending on the
change in residual volume after partial expiration (RVpart).
Bronchial Challenges
Solutions of MCh were prepared by adding distilled water to dry powder MCh chloride (Laboratorio Farmaceutico Lofarma, Milan, Italy). Aerosols were delivered by a SM-1 Rosenthal breath-activated dosimeter (SensorMedics) driven by compressed air (30 lb./in.2) with 1-s actuations. Aerosol output at the mouth was 10 µl per actuation. Aerosols were inhaled during quiet tidal breathing in a sitting position.On screening day, the doses of MCh causing a reduction of sGaw by 35%
(PD35sGaw) or FEV1 by 20%
(PD20FEV1) were determined by standard
incremental challenges. After 20 tidal inhalations of saline as a
control, subjects inhaled double-increasing doses of MCh from 0.01 mg
until a decrement of sGaw of 
35% or of FEV1 of 20%
was recorded 2 min after dosing. Dose increments were obtained by using
three MCh concentrations (1, 10, and 50 mg/ml) with appropriate numbers
of breaths (from 1 to 16). PD35sGaw and PD20FEV1 were calculated by interpolating
between two adjacent points of log dose-response curves.
Experimental Procedures
Study 1.
On 2 separate study days and in a random order, 10 asthmatic and 8 healthy subjects (Table 1) inhaled a single dose of MCh equal to twice
the last dose inhaled in the standard incremental challenge to obtain
the PD20FEV1, not preceded (day 1)
or preceded (day 2) by five deep breaths (Fig.
1). The inhalation time lasted ~1 min.
sGaw, FRC, part, RVpart, FEV1, and FVC were measured in triplicate before a 10-min prohibition of deep breaths, whereas single measurements of sGaw, FRC, part, and RVpart were taken again immediately before MCh inhalation. All measurements were then
taken once at 1 and 10 min after MCh inhalation. Means of the
triplicate measurement of sGaw, part, RVpart, and FRC and the
best FEV1-FVC combination were used as baseline values. In all circumstances, the full expiratory maneuver to measure
FEV1 and FVC was preceded by measurement of sGaw, FRC, and
partial expiratory maneuvers. Spontaneous deep breaths or sighs were
strictly prohibited from 10 min before to 10 min after MCh inhalation.
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Study 2.
On 2 separate study days and in a random order, 16 asthmatic and 6 healthy subjects (Table 1) inhaled for ~1 min a single dose of MCh,
equal to twice the last dose used in the standard incremental challenge
to obtain the PD35sGaw, not preceded (day 1) or
preceded (day 2) by five deep breaths (Fig. 1).
PD35sGaw was used because PD20FEV1
in study 1 caused very large changes of all parameters not
preceded by deep breath, which might have minimized or masked
differences between conditions. sGaw, FRC, part, RVpart,
FEV1, and FVC were measured in triplicate before a 10-min
prohibition of deep breaths, whereas single measurements of sGaw, FRC,
part, and RVpart were taken again immediately before MCh
inhalation. Means of the triplicate measurement of sGaw, part,
RVpart, and FRC were taken as baseline values. Measurements of sGaw and
FRC (and also of part and RVpart in 8 asthmatic subjects) were
taken every minute for the first 10 min and then at 15, 20, and 40 min
after MCh inhalation. Spontaneous deep breaths or sighs were strictly
prohibited during the entire test.
Statistical Analysis
A mixed between-within groups ANOVA with Duncan's post hoc comparisons was used for both studies. For study 1, the dependent variables were the percent changes of FEV1, FVC, FRC,part, RVpart, and sGaw, whereas groups, study days, and
observation times were the independent factors. For study 2,
the dependent variables were the areas under the curves (AUC) of
percent changes in part and sGaw or the absolute changes in FRC
and RVpart vs. time, whereas groups and study days were the independent
factors. Values of P < 0.05 were considered
statistically significant. Data are presented as means ± SD.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Study 1
There were no significant differences in baseline lung function between study days (Table 2). Furthermore, there were no significant differences in FRC,part,
RVpart, and sGaw before and after the 10-min deep-breath prohibition
(P > 0.1 for all comparisons).
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In the healthy subjects (Fig.
2A), the decrements of
FEV1 and FVC induced by MCh inhalation on the day without
deep breaths were 37 ± 14 and 28 ± 15% after 1 min,
respectively, and 37 ± 13 and 28 ± 14% after 10 min,
respectively. On the day with five deep breaths, the decreases of both
FEV1 (27 ± 13%) and FVC (13 ± 9%) were
significantly less (P < 0.05 and P < 0.01, respectively) after 1 min, but not after 10 min (35 ± 17%
for FEV1 and 28 ± 14% for FVC), than on the day
without deep breaths . By contrast, the increments in RVpart and FRC
and the decrements of sGaw and part were similar with or without
the deep breaths at either 1 or 10 min after MCh (P > 0.4 for all comparisons).
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In the asthmatic subjects (Fig. 2B), there were no
significant differences in decrements of FEV1, FVC, sGaw,
and part, or in increments in RVpart and FRC between days with
and without deep breaths, either after 1 or 10 min (P > 0.1 for all comparisons).
Study 2
Mean baseline sGaw and FRC were not significantly different between study days either in asthmatic or healthy subjects (Table 3). Furthermore, there were no significant differences in FRC, sGaw,part, and RVpart
before and after the 10-min deep-breath prohibition (P > 0.1 for all comparisons).
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The decrease of sGaw over time (Fig. 3)
was greater on the day with than on the day without deep breaths, both
in asthmatic (AUC: 1,970 ± 651 vs. 1,395 ± 612) and healthy
(AUC: 1,485 ± 475 vs. 1,053 ± 403) subjects. Although the
difference between study days achieved statistical significance
(P < 0.01) only in the asthmatic group, there was no
significant interaction between study days and groups
(P = 0.6), suggesting that the effect of the deep
breaths was not significantly different in the two groups. Similarly,
the increase of FRC (Fig. 4) over time
was greater on the day with than on the day without deep breaths in
asthmatic subjects (AUC: 13.89 ± 11.03 vs. 5.34 ± 7.07, P < 0.01) and at several times in the healthy
group (AUC: 5.34 ± 3.83 vs. 2.03 ± 5.70, P = 0.05). As for sGaw, there was no significant interaction between
study days and groups (P > 0.2).
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In the subgroup of asthmatic subjects in whom part and RVpart
were also measured, the percent decrease of part (Fig.
5A) and the absolute increase
in RVpart (Fig. 5B) over time were significantly greater on
the day with than on the day without deep breaths (part: AUC,
2,526 ± 648 vs. 1,939 ± 570, P < 0.05;
RVpart: AUC, 26.57 ± 16.3 vs. 7.88 ± 3.20, P < 0.05).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The results of the present study can be summarized as follows. First, the bronchoprotective effect of deep breaths taken before a single dose of MCh was only visible in healthy subjects by using parameters preceded by full inflation (FEV1 and FVC). Second, prior deep breaths enhanced the bronchoconstrictor response to MCh in both healthy and asthmatic subjects, as inferred from changes in parameters not requiring full lung inflation.
Two recent studies (10, 21) reported that a series of five deep breaths taken before the inhalation of a single dose of MCh dramatically and exclusively protected healthy humans from airway narrowing. The conclusion was based on the fact that the decrements of FEV1 and FVC after a bolus of MCh were significantly less when the constrictor agent was preceded by deep breaths than when it was not. The results of the present study confirm that prior deep breaths significantly blunt the decrease of FEV1 and FVC measured 1 min after MCh in healthy subjects, and this protective effect is absent in asthmatic patients. A new finding is that the deep breaths had no effects on changes in FEV1 and FVC measured 10 min after MCh inhalation even in healthy subjects.
The bronchoprotective effect of deep breaths observed in healthy
subjects by Kapsali et al. (10) was interpreted as
suggesting a depression of the airway smooth muscle contractile
machinery at the levels of the cross-bridge cycling rate
(3) or plastic adaptation of the contractile filaments
within the smooth muscle cell (5). The fact that
FEV1 and FVC decreased less when MCh was preceded by deep
breaths than when it was not does not, however, necessarily imply a
reduced capacity of airway smooth muscle to shorten because of the
possible effects of the full lung inflation required by these
measurements. The finding of study 1 that the deep breaths
blunted the decrease of FEV1 and FVC but not of
measurements not preceded by a full inflation, such as part,
RVpart, FRC, and sGaw, suggests a mechanism facilitating the
distensibility of contracted airways rather than inhibiting airway
smooth muscle shortening. In healthy subjects, the disappearance of the
effect of prior deep breaths on the decrease of FEV1 and
FVC after 10 min of prohibition of further deep breaths may reflect a
progressive increase in airway smooth muscle stiffness when the
contractile apparatus is no more urged to change configuration with
large lung inflations (3, 5). This is consistent with in
vitro data showing that the tone of airway smooth muscle is fully
recovered under static conditions within 8 min after a large stretch
(4). The difference in the effect of the deep breaths on
FEV1 and FVC between healthy and asthmatic subjects, but
not on the parameters not preceded by a full inflation, may be
interpreted as reflecting greater airway stiffness in asthma (7,
8). According to the latch-bridge theory (15),
unstretched airway smooth muscle goes into a "frozen" state
characterized by less hysteresivity and greater stiffness
(3). Therefore, a reduced ability of the full inflations
to distend constricted airways would reflect a greater proportion of
latch bridges formed in asthma during prohibition of the deep
inspirations preceding MCh inhalation. In healthy subjects, the
multiple deep breaths would convert more latch bridges into rapidly
cycling cross bridges, thus increasing airway smooth muscle
hysteresivity and distensibility (3). Another theory that
can explain a reduced stiffness after the deep breaths is a change in
the configuration of the contractile elements inside the cell from a
parallel to a serial arrangement (5). Whether the
cytoskeletal configuration of asthmatic airway smooth muscle is
different from normal is, however, unknown. Alternative hypotheses that
possibly help explain these findings are a prevalent distribution of
airway obstruction in the most peripheral parts of the lung
(1) and more extensive airway closure (9), as well as a decreased airway-to-parenchyma interdependence in asthmatic compared with normal subjects (6). All of these functional conditions are expected to require extra distending forces to achieve a
given degree of bronchodilatation.
Another important finding of this study is that deep breaths taken
before inhalation of MCh enhanced the bronchoconstrictor response, as
assessed by any parameter not preceded by a full lung inflation (FRC,
part, RVpart, and sGaw) recorded over time after MCh. This
effect was similar in healthy and asthmatic subjects. The data of the
present study do not allow us to give a conclusive explanation for this
finding, but some speculation can be made about possible mechanisms. In
some asthmatic patients, a sustained bronchoconstriction may develop
after taking one or more full inflations (13, 18), an
effect that has been attributed to a myogenic response triggered by the
stretching of airway smooth muscle (22, 23). In vitro,
this behavior was observed after passive sensitization with allergic
serum (14) or chemical agents able to convert airway
smooth muscle from multiunit to single-unit conditions
(23). In vivo, this phenomenon seems to occur only in a
minority of subjects with rather severe asthma. In the present study,
no subject showing even a slight decrease in sGaw after five deep
breaths was included. This and the observation that the deep breaths
taken before MCh inhalation tended to increase the bronchoconstrictor
response even in normal subjects seem to rule out a myogenic response
as a major determinant of the present findings. Nevertheless, we
acknowledge that mechanical stretching can increase the permeability of
the smooth muscle cell membrane to ions, including calcium (2,
11), and in addition cause release of mediators and/or
activation of neural pathways. Although not perhaps sufficient to
trigger a contractile response in unstimulated smooth muscle, these
mechanisms could interfere with the response to MCh. In this
scenario, the net effect of the deep breaths would result from the
balance between mechanisms causing airway smooth muscle contraction and
mechanisms causing bronchodilatation. Alternatively, the greater
response to MCh after the series of deep breaths might have been due to
mechanical unloading of the airways. Because of imperfect rheological
properties, the elastic recoil of lung parenchyma decreases after a
deep inspiration and needs time to recover (20).
Therefore, the external load on airway smooth muscle will be
transiently reduced after a deep breath. If multiple deep breaths cause
a steplike reduction of lung elastic recoil, then the airway smooth
muscle might be even more unloaded and for a longer time. Therefore,
when tidal breathing is resumed after the deep breaths, the cyclic
stretching imposed by lung parenchyma is less, thus possibly resulting
in more rapid transition to a frozen state (3) or
adaptation of the contractile apparatus to a shorter length
(4). Under these conditions, exposure of the airways to a
constrictor agent followed by a long prohibition of deep breaths after
MCh could have resulted in greater airway narrowing. Finally, we
acknowledge that a series of deep breaths before a constrictor agent
may have increased mucosal permeability to the agent itself, thus
causing an increased response similarly in both groups.
In the subgroup of asthmatic subjects in whom part and RVpart
were also measured, the same enhancing effect of deep breaths on airway
narrowing was observed as with sGaw and FRC. This rules out that the
effect of deep breaths on MCh-induced changes in sGaw was limited to
large or extrathoracic airways. The consistently greater decrements in
part and sGaw and the increments in RVpart and FRC when MCh was
preceded by five deep breaths would suggest enhanced airway narrowing
both downstream and upstream from the flow-limiting segment, greater
airway closure, and remarkable lung hyperinflation as a reaction of the
respiratory system to airway narrowing.
An additional observation that may have practical implications is that, in healthy subjects, the decrease of FEV1 with a single MCh dose equal to twice the last dose used to obtain the PD20FEV1 was much greater than 20% when the deep breaths were prohibited. This difference probably reflects the protective effect of the multiple full inflation maneuvers made to measure FEV1 during the standard cumulative challenge on the screening day.
In conclusion, the present study reveals new and more complex features of airway responses to repeated deep breaths. In both asthmatic and healthy subjects, deep breaths taken before inhaling MCh surprisingly enhanced the bronchoconstrictor response. The major difference between healthy and asthmatic subjects in this respect seems to be the ability of the deep breaths to increase the distensibility of contracted airways in healthy patients.
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ACKNOWLEDGEMENTS |
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The authors thank Giacomo Spano for valuable technical assistance.
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FOOTNOTES |
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This study was supported in part by Ministero dell'Istruzione, dell'Universitá della Ricerca, Rome, Italy.
Address for reprint requests and other correspondence: V. Brusasco, Dipartimento di Medicina Interna, Università di Genova, Viale Benedetto XV, 6, 16132 Genova, Italy (E-mail: brusasco{at}dism.unige.it).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
June 21, 2002;10.1152/japplphysiol.00209.2002
Received 12 March 2002; accepted in final form 20 June 2002.
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REFERENCES |
|---|
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Burns, CB,
Taylor WR,
and
Ingram RH, Jr.
Effect of deep inhalation in asthma: relative airway and parenchymal hysteresis.
J Appl Physiol
59:
1590-1596,
1985.
2.
Coburn, RF.
Stretch-induced membrane depolarization in ferret trachealis smooth muscle cells.
J Appl Physiol
62:
2320-2325,
1987.
3.
Fredberg, JJ,
Inouye D,
Miller B,
Nathan M,
Jafari S,
Raboundi SH,
Butler JP,
and
Shore SA.
Airway smooth muscle, tidal stretches, and dynamically determined contractile states.
Am J Respir Crit Care Med
156:
1752-1759,
1997.
4.
Gunst, SJ.
Contractile force of canine airway smooth muscle during cyclical length changes.
J Appl Physiol
55:
759-769,
1983.
5.
Gunst, SJ,
and
Wu MF.
Selected contribution: plasticity of airway smooth muscle stiffness and extensibility: role of length-adaptive mechanisms.
J Appl Physiol
90:
741-749,
2001.
6.
Irvin, CG,
Pak J,
and
Martin RJ.
Airway-parenchyma uncoupling in nocturnal asthma.
Am J Respir Crit Care Med
161:
50-56,
2000.
7.
Jensen, A,
Atileh H,
Suki B,
Ingenito EP,
and
Lutchen KR.
Selected contribution: airway caliber in healthy and asthmatic subjects: effect of bronchial challenge and deep inspiration.
J Appl Physiol
91:
506-515,
2001.
8.
Johns, DP,
Wilson J,
Harding R,
and
Walters EH.
Airway distensibility in healthy and asthmatic subjects: effect of lung volume history.
J Appl Physiol
88:
1413-1420,
2000.
9.
Kaminsky, DA,
Bates JHT,
and
Irvin CG.
Effects of cool, dry air stimulation on peripheral lung mechanics in asthma.
Am J Respir Crit Care Med
162:
179-186,
2000.
10.
Kapsali, T,
Permutt S,
Laube B,
Scichilone N,
and
Togias A.
Potent bronchoprotective effect of deep inspiration and its absence in asthma.
J Appl Physiol
89:
711-720,
2000.
11.
Liu, M,
Xu J,
Tanswell B,
and
Post M.
Inhibition of strain-induced fetal rat lung cell proliferation by gadolinium, a stretch activated channel blocker.
J Cell Physiol
161:
501-507,
1994.
12.
Malmberg, P,
Larsson K,
Sundblad BM,
and
Zhiping W.
Importance of the time interval between FEV1 measurements in a methacholine provocation test.
Eur Respir J
6:
680-686,
1993.
13.
Marthan, R,
and
Woolcock AJ.
Is a myogenic response involved in deep inspiration-induced bronchoconstriction in asthmatics?
Am Rev Respir Dis
140:
1354-1358,
1989.
14.
Mitchell, RW,
Rabe KF,
Magnussen H,
and
Leff AR.
Passive sensitization of human airways induces myogenic contractile responses in vitro.
J Appl Physiol
83:
1276-1281,
1997.
15.
Murphy, RA.
What is special about smooth muscle? The significance of covalent crossbridge regulation.
FASEB J
8:
311-318,
1994.
16.
National Heart, Lung, and Blood Institute.
Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention. NHLBI/WHO Workshop Report. Bethesda, MD: National Institutes of Health, 1995. (Publ. 95-3659)
17.
Pellegrino, R,
Sterk P,
Sont JK,
and
Brusasco V.
Assessing the effect of deep inhalation on airway calibre: a novel approach to lung function in bronchial asthma and COPD.
Eur Respir J
12:
1219-1227,
1998.
18.
Pellegrino, R,
Violante B,
Crimi E,
and
Brusasco V.
Time course and calcium dependence of sustained bronchoconstriction induced by deep inhalation in asthma.
Am Rev Respir Dis
144:
1262-1266,
1991.
19.
Quanjer, PH,
Tammeling GJ,
Cotes JE,
Pedersen OF,
Peslin R,
and
Yernault JC.
Standardized lung function testing.
Eur Respir J
6:
1-99,
1993.
20.
Rodarte, JR,
Noredin G,
Miller C,
Brusasco V,
and
Pellegrino R.
Lung elastic recoil during breathing at increased lung volume.
J Appl Physiol
87:
1491-1495,
1999.
21.
Scichilone, N,
Kapsali T,
Permutt S,
and
Togias A.
Deep inspiration-induced bronchoprotection is stronger than bronchodilation.
Am J Respir Crit Care Med
162:
910-916,
2000.
22.
Stephens, NL.
Postjunctional factors in airway smooth muscle hyperresponsiveness.
In: Handbook of Physiology. The Respiratory System. Mechanics of Breathing. Bethesda, MD: Am. Physiol. Soc, 1986, sect. 3, vol. III, pt. 2, chapt. 41, p. 719-726.
23.
Stephens, NL,
Kroeger EA,
and
Kromer U.
Induction of a myogenic response in tonic airway smooth muscle by tetraethylammonium.
Am J Physiol
228:
628-632,
1975.
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P. B. Noble, P. K. McFawn, and H. W. Mitchell Intraluminal pressure oscillation enhances subsequent airway contraction in isolated bronchial segments J Appl Physiol, March 1, 2004; 96(3): 1161 - 1165. [Abstract] [Full Text] [PDF]
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V. Brusasco and R. Pellegrino Invited Review: Complexity of factors modulating airway narrowing in vivo: relevance to assessment of airway hyperresponsiveness J Appl Physiol, September 1, 2003; 95(3): 1305 - 1313. [Abstract] [Full Text] [PDF]
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P < 0.01.
) or not preceded
(solid lines, 
) by 5 deep breaths. Data are means ± SD. Areas under the curves were significantly greater with than
without the 5 deep breaths (P < 0.05) with no
significant difference between healthy and asthmatic subjects
(P = 0.6).
