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1 response that leads to airway constriction (bronchoconstriction).
2 ing in efferent vagal activity and asthmatic bronchoconstriction.
3 24 h duration of action in a mouse model of bronchoconstriction.
4 though inhaled iloprost occasionally induced bronchoconstriction.
5 and 10%, respectively, consistent with acute bronchoconstriction.
6 a that contribute to airway inflammation and bronchoconstriction.
7 aoperative reactions such as hypotension and bronchoconstriction.
8 ne release and potentiating vagally mediated bronchoconstriction.
9 antify global gas exchange impairment during bronchoconstriction.
10 3 also mediate the calcium response and thus bronchoconstriction.
11 inergic-mediated pathways contributed to the bronchoconstriction.
12 revenal, a natural antagonist, inhibited the bronchoconstriction.
13 ients with CHF and COPD for fear of inducing bronchoconstriction.
14 ism and saline lung lavage and bimodal after bronchoconstriction.
15 ricular tachycardias without hypotension and bronchoconstriction.
16 helium, contributed to both inflammation and bronchoconstriction.
17 es a variety of reflexes including cough and bronchoconstriction.
18 d to the increase in respiratory work during bronchoconstriction.
19 halational anesthetics because of refractory bronchoconstriction.
20 , a similar role of Rac1 was observed during bronchoconstriction.
21 ch is the acute compressive stress caused by bronchoconstriction.
22 2 antagonists may be useful drugs to prevent bronchoconstriction.
23 est a novel pathway by which AQP5 influences bronchoconstriction.
24 ion of M1 and M3 muscarinic receptors causes bronchoconstriction.
25 )-agonists are widely used for the relief of bronchoconstriction.
26 ypercapnia only during moderate, not severe, bronchoconstriction.
27 provides protection against exercise-induced bronchoconstriction.
28 a) and pH 6.87+/-0.11) developed with severe bronchoconstriction.
29 n patients with congestive heart failure and bronchoconstriction.
30 termine whether activation of RARs can cause bronchoconstriction.
31 Hypertonic saline (HTS) induces bronchoconstriction.
32 n-induced changes in ASF osmolality initiate bronchoconstriction.
33 s been suggested as a potential modulator of bronchoconstriction.
34 nts can cause dyspnoea, chest discomfort and bronchoconstriction.
35 tion, and inhibit antigen-induced late-phase bronchoconstriction.
36 vivo efficacy reducing early and late phase bronchoconstriction.
37 infections increase vagally mediated reflex bronchoconstriction.
38 otect such patients against exercise-induced bronchoconstriction.
39 ation, plasma leakage, leukocyte influx, and bronchoconstriction.
40 es in the lung, potentiating vagally induced bronchoconstriction.
41 tion (DI) to total lung capacity may lead to bronchoconstriction.
42 asthmatic subjects to monitor for excessive bronchoconstriction.
43 kg) and 82% (5 mg/kg) inhibition of allergic bronchoconstriction.
44 g dose of zafirlukast attenuated SO2-induced bronchoconstriction.
45 h or 3 wk BAL, but did not affect the acute bronchoconstriction.
46 docaine at blocking histamine-induced reflex bronchoconstriction.
47 administered to prevent this reflex-induced bronchoconstriction.
48 of acetylcholine, inhibiting vagally induced bronchoconstriction.
49 d intravenous lidocaine block reflex-induced bronchoconstriction.
50 66, however, did not block histamine-induced bronchoconstriction.
51 rapeutic serum concentrations blocked reflex bronchoconstriction.
52 pilocarpine's inhibition of vagally induced bronchoconstriction.
53 reduces acetylcholine- and serotonin-induced bronchoconstriction.
54 inhaled amitriptyline directly reduces acute bronchoconstriction.
55 target to reduce allergen-induced asthmatic bronchoconstriction.
56 he defining diagnostic feature is mechanical bronchoconstriction.
57 ed the inhibitory effect of amitriptyline on bronchoconstriction.
58 ells, leading to lethal vascular leakage and bronchoconstriction.
59 ed nitric oxide (FENO) levels decrease after bronchoconstriction.
60 target to reduce allergen-induced asthmatic bronchoconstriction.
61 ient mice, with evident vascular leakage and bronchoconstriction.
62 ogical RhoA-dependent Ca(2+) sensitivity and bronchoconstriction.
63 Lung nociceptors initiate cough and bronchoconstriction.
64 rin induce IL-33-dependent MC activation and bronchoconstriction.
65 al response to beta(2) agonists resulting in bronchoconstriction.
66 and control of asthma symptoms by reversing bronchoconstriction.
67 y included 13 patients with exercise-induced bronchoconstriction.
68 er studies of patients with exercise-induced bronchoconstriction.
69 eshold concentrations of allergen to produce bronchoconstriction.
70 duced airway inflammation, eosinophilia, and bronchoconstriction.
71 ves, which upon activation can elicit reflex bronchoconstriction.
72 inspirations are less effective in reversing bronchoconstriction.
73 esponse to histamine, without inhibiting the bronchoconstriction.
74 cetylcholine release and potentiating reflex bronchoconstriction.
75 l activity of nodose C-fibres in response to bronchoconstriction.
76 ted heparins attenuate antigen-induced acute bronchoconstriction, (2) nonanticoagulant fractions medi
78 asthma frequently have only exercise-induced bronchoconstriction, a symptom of inadequate control of
80 ave demonstrated that normal infants exhibit bronchoconstriction after inhalation of nonspecific agon
81 ve cigarette smoke) have more wheeze, cough, bronchoconstriction, airway hyper-reactivity and mucous
82 n of heparin (LA-heparin) on antigen-induced bronchoconstriction, airway hyperresponsiveness (AHR), a
83 responses in human airways in vivo, such as bronchoconstriction, airway hyperresponsiveness and infl
84 nhibits allergen-induced responses including bronchoconstriction, airway hyperresponsiveness, and inf
85 ma, including bronchial hyperresponsiveness, bronchoconstriction, airway inflammation, and airway rem
86 ing, nasal congestion, rhinorrhea, coughing, bronchoconstriction, airway mucus secretion, dysphagia,
87 late central and local reflex events such as bronchoconstriction, airway plasma leakage, mucus secret
88 us area of high tracer retention (TR) during bronchoconstriction and a second one covering an area of
89 reduction in regional Q to the TR ROI during bronchoconstriction and a variable and nonsignificant ch
90 ympathetic signaling leads to hyperactivated bronchoconstriction and abnormal respiration in the KO n
91 ficacy against exercise and allergen-induced bronchoconstriction and additive benefit for use in pati
93 nificantly blocks antigen-induced late-phase bronchoconstriction and airway hyper-responsiveness in s
94 gest tryptase involvement in both late-phase bronchoconstriction and airway hyperreactivity and furth
95 esults indicate that inhaled tryptase causes bronchoconstriction and airway hyperresponsiveness in al
98 y of airway disease, plays a central role in bronchoconstriction and airway remodeling, including air
99 he synthesis of leukotrienes which can cause bronchoconstriction and airways edema and appear to be i
100 lective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sensitive individuals.
102 eive the same quality of dyspnea during mild bronchoconstriction and external resistive loads, we stu
103 rasympathetic nerves causes vagally mediated bronchoconstriction and hyperresponsiveness following an
104 atment with AMG 157 reduced allergen-induced bronchoconstriction and indexes of airway inflammation b
105 efficacy and duration of action in both the bronchoconstriction and inflammation assays in rat after
106 balanced MAPI lead compound, as assessed in bronchoconstriction and inflammation assays in rats afte
107 mast cells has been implicated in the severe bronchoconstriction and inflammation prevalent in these
108 Inhaled heparin prevents antigen-induced bronchoconstriction and inhibits anti-IgE-mediated mast-
109 LT receptor or 5-lipoxygenase, implying that bronchoconstriction and MC activation were both cysLT de
112 e certain mechanisms to specific patterns of bronchoconstriction and subsequently match phenotypes of
113 strically), significantly inhibited both the bronchoconstriction and the eosinophilia at 24 h, wherea
115 A(3) adenosine receptor to adenosine-induced bronchoconstriction and to assess the contribution of ma
116 etermine: (1) if aerosolized tryptase causes bronchoconstriction, and (2) the mechanism by which this
117 dose-dependent inhibition of antigen-induced bronchoconstriction, and a 5-mg/kg nebulized dose caused
118 y chronic pulmonary inflammation, reversible bronchoconstriction, and airway hyperreactivity to provo
123 dioxide (SO(2) ) triggers coughs and reflex bronchoconstriction, and stimulation of vagal bronchopul
125 tion and in AHR, but no changes in immediate bronchoconstriction as compared with control recipients.
126 ivation of parasympathetic signaling-induced bronchoconstriction, as evidenced by increased pulmonary
127 herapy for the treatment of inflammation and bronchoconstriction associated with persistent asthma is
129 dose of salmeterol attenuated the degree of bronchoconstriction at all times (decrease in FEV1 on da
130 ed consistent inhibition of exercise-induced bronchoconstriction at the end of the 8-week dosing inte
132 ral infections may increase vagally mediated bronchoconstriction both by directly inhibiting M2 recep
133 mographic lung imaging at baseline and after bronchoconstriction, breathing either room air or 80% ox
134 ge in serum recipients resulted in immediate bronchoconstriction but had no effect on AHR or on pulmo
135 ng and deep inspirations potently antagonize bronchoconstriction, but in the asthmatic lung this salu
136 this response, the antagonism of SO2-induced bronchoconstriction by a single oral dose of the leukotr
138 nsteroidal anti-inflammatory drug-associated bronchoconstriction by challenging aspirin-exacerbated r
139 t chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair te
140 lume was increased equally in the absence of bronchoconstriction by increasing end-expiratory pressur
141 demonstrate that IL-33 exacerbates allergic bronchoconstriction by increasing synthesis, storage, an
145 airway smooth muscle also appear to mediate bronchoconstriction caused by the muscarinic receptor ag
146 onses that influence cardiorenal, pulmonary (bronchoconstriction), central nervous system (locomotion
147 during 92% of the 26 trials of methacholine bronchoconstriction compared with 3% of the 72 trials of
148 rway PGE2 levels, and augmented GPCR-induced bronchoconstriction compared with either RGS4 KO mice or
149 e ablation of sensory neurons does not limit bronchoconstriction, constriction after Ag challenge is
150 he airway wall into a rosette pattern during bronchoconstriction creates a complex stress field, with
153 the postbronchodilator baseline ("excessive bronchoconstriction") during their first sputum inductio
154 clin (IP) also enhanced the mannitol-induced bronchoconstriction (E(max), 67% +/- 5%, 66% +/- 4%, and
156 the treatment of choice for exercise-induced bronchoconstriction (EIB) and act through specific recep
160 ical research supports that exercise-induced bronchoconstriction (EIB) is caused by hyperosmolar trig
162 methacholine challenge and exercise-induced bronchoconstriction (EIB) test (n = 478) at 10 years and
169 stic recoil and interdependence during acute bronchoconstriction episodes may predispose the HFEV(1)
170 reactivity, whereas WT mice developed marked bronchoconstriction following aerosol Ag sensitization a
171 Thus, in the mouse the initial period of bronchoconstriction following allergen exposure may invo
172 if heparin inhibits hyperventilation-induced bronchoconstriction (HIB) in a canine model of EIA, and
173 activity modulates hyperventilation-induced bronchoconstriction (HIB) in canine peripheral airways a
175 Our findings show that HA blocks PPE-induced bronchoconstriction in a dose-dependent and molecular we
178 rograms albuterol does not prevent excessive bronchoconstriction in all asthmatic subjects undergoing
180 ptor (beta2-AR)-agonists are used to relieve bronchoconstriction in asthma, but may reduce asthma con
181 led beta-agonists are effective at reversing bronchoconstriction in asthma, but the mechanism by whic
182 scle (ASM)-relaxing agents that help reverse bronchoconstriction in asthma, but their ability to affe
186 with des-Arg10-lysylbradykinin did not cause bronchoconstriction in asthmatic subjects or increase gl
189 gonist pilocarpine inhibited vagally-induced bronchoconstriction in control but not challenged animal
190 onchoprotection against methacholine-induced bronchoconstriction in guinea pig lung slices, but - in
193 aintained for a prolonged period after acute bronchoconstriction in humans in the absence of deep ins
194 ene receptor (CysLT(1)R) are efficacious for bronchoconstriction in humans with bronchial asthma; how
197 ETS increases citric acid-induced cough and bronchoconstriction in part by an NK-1 receptor mechanis
199 ntilation of hot humid air induces transient bronchoconstriction in patients with asthma; the underly
200 offsets non-selective beta blockade-induced bronchoconstriction in patients with obstructive airway
201 , activation of airway mast cells (MCs), and bronchoconstriction in response to nonselective cyclooxy
202 led porcine pancreatic elastase (PPE) causes bronchoconstriction in sheep via a bradykinin-mediated m
203 ously shown that heparin attenuates allergic bronchoconstriction in sheep, inhibits anti-IgE mediated
206 by 99%, at an oral dose of 10 mg/kg, and the bronchoconstriction in the allergic guinea pig by 50%, a
207 hallenge evoked a significantly more intense bronchoconstriction in the Ova-sensitized group (control
208 aproxen, diclofenac, or ibuprofen) increased bronchoconstriction in tissue from wild-type but not fro
209 ry activity and long duration of action in a bronchoconstriction in vivo model in mice via intranasal
210 tory activity and long duration of action in bronchoconstriction in vivo models in two species via in
211 osure enhances citric acid-induced cough and bronchoconstriction in young guinea pigs via a neurokini
212 e high levels of IgE antibody and experience bronchoconstriction, increased airway hyperresponsivenes
216 nto murine airways abrogated the exaggerated bronchoconstriction induced by allergen sensitization an
217 d short-term prophylactic protection against bronchoconstriction induced by exercise or other stimuli
219 was designed to test the hypothesis that the bronchoconstriction induced by increasing airway tempera
220 P2X2/3 purinoceptor antagonists, blocked the bronchoconstriction-induced nodose C-fibre discharge.
227 view, we show herein that mast cell-mediated bronchoconstriction is observed only in animals with int
231 Here we present experimental evidence that bronchoconstriction leads to patchiness in lung ventilat
232 room air and 80% O2 conditions (baseline vs. bronchoconstriction, mean +/- SD, 1.02 +/- 0.20 vs. 0.35
233 f ventilation-perfusion (VA/Q) ratios during bronchoconstriction measured with the multiple inert gas
234 , released from activated mast cells, causes bronchoconstriction mediated by H(1) receptors, whereas
235 and pH 7.28+/-0.02) developed with moderate bronchoconstriction; more profound respiratory acidosis
236 are important mediators of asthma by causing bronchoconstriction, mucous secretion, and increased vas
237 sLTs) are potent lipid mediators involved in bronchoconstriction, mucus secretion, and cell trafficki
238 ntilated sheep before and after methacholine bronchoconstriction (n = 3) and pulmonary embolism (n =
240 e by Ascaris suum) abolished both late-phase bronchoconstriction (no significant increase in specific
243 occurred in the healthy subjects but further bronchoconstriction occurred in the subjects with asthma
244 at PAR2 agonists, including tryptase, induce bronchoconstriction of human airway by stimulating smoot
245 nflammation and AHR in mice and also reduced bronchoconstriction of human airway samples in vitro.
246 n and overperception assessed during induced bronchoconstriction or bronchodilation or during changes
247 l and nonpharmaceutical) of exercise-induced bronchoconstriction or exercise-induced asthma (which is
248 often characterized by an initial period of bronchoconstriction, or early phase reaction (EPR), that
249 s characterized by airway epithelial damage, bronchoconstriction, parenchymal destruction and mucus h
251 P released within the tissues in response to bronchoconstriction plays a pivotal role in the mechanic
255 gs inhibit LTD4-, LTE4-, and antigen-induced bronchoconstriction, reduce inflammatory markers in mode
256 that the bimodality of VA/Q distributions in bronchoconstriction reflects the involvement of large co
257 t therapeutic approaches to avoid or reverse bronchoconstriction rely primarily on B2 adrenoceptor ag
259 20 to -69%); no subject developed refractory bronchoconstriction requiring hospitalization or emergen
260 eatment, and no subject developed refractory bronchoconstriction requiring treatment other than rever
261 nists, PGE2 inhibited the mast cell-mediated bronchoconstriction resulting from anti-IgE challenge.
262 y defense responses such as cough and reflex bronchoconstriction, resulting from activation of vagal
263 n as well as directly cause vasodilation and bronchoconstriction, resulting in anaphylaxis-like react
264 y and expression of a mediator of endogenous bronchoconstriction, S-nitrosoglutathione (GSNO) reducta
265 ough the measurement of airway inflammation, bronchoconstriction, serum IgE levels, and bronchoalveol
266 d suggest that both ISH and allergen-induced bronchoconstriction share pathobiologic mechanisms that
267 ay be an additional mechanism for decreasing bronchoconstriction, since it would decrease eosinophil
269 greater protection against exercise-induced bronchoconstriction than placebo therapy (expressed as t
271 way, and kallikrein, which mediates allergic bronchoconstriction that limits the inhalation of noxiou
272 primary question is how they are related to bronchoconstriction, the main clinical feature of asthma
273 rienes (cysLTs) mediate vascular leakage and bronchoconstriction through the smooth muscle-associated
274 people worldwide, is defined by exaggerated bronchoconstriction to inflammatory mediators including
275 nificantly increased concentration-dependent bronchoconstriction to intravenously administered Ach, a
276 al stress similar to that experienced during bronchoconstriction triggers epithelial cell signaling t
277 of the reduction in relative perfusion after bronchoconstriction under 80% O2 conditions occurred as
278 w region, relative perfusion decreased after bronchoconstriction under room air conditions and also,
281 n combination with immunohistochemistry, and bronchoconstriction was assessed by whole body plethysmo
285 xposed to mechanical compression that mimics bronchoconstriction, we find that compression induces Hi
290 e prebronchodilator FEV1 > 80% had excessive bronchoconstriction, whereas 10 of the 24 subjects (42%)
291 zed dose caused a 67% inhibition of allergic bronchoconstriction, whereas a 2.5-mg/kg dose was ineffe
293 rways of asthmatic individuals causes severe bronchoconstriction, which is in part neurally mediated
294 neural control of the airways contribute to bronchoconstriction, which is reflected in an increased
295 ors by gallamine potentiated vagally induced bronchoconstriction, while in challenged animals this ef
296 ized guinea pigs, 47.Na dosed orally blocked bronchoconstriction with an ED(50) = 0.4 mg/kg, the most
297 ly to be far more common than is symptomatic bronchoconstriction with beta(2) agonists, but no system
299 main components of asthma (inflammation and bronchoconstriction) with fluticasone propionate and sal