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1 response that leads to airway constriction (bronchoconstriction).
2 , a similar role of Rac1 was observed during bronchoconstriction.
3 and 10%, respectively, consistent with acute bronchoconstriction.
4 a that contribute to airway inflammation and bronchoconstriction.
5 aoperative reactions such as hypotension and bronchoconstriction.
6 ne release and potentiating vagally mediated bronchoconstriction.
7 antify global gas exchange impairment during bronchoconstriction.
8 3 also mediate the calcium response and thus bronchoconstriction.
9 inergic-mediated pathways contributed to the bronchoconstriction.
10 revenal, a natural antagonist, inhibited the bronchoconstriction.
11 ients with CHF and COPD for fear of inducing bronchoconstriction.
12 ism and saline lung lavage and bimodal after bronchoconstriction.
13 ricular tachycardias without hypotension and bronchoconstriction.
14 helium, contributed to both inflammation and bronchoconstriction.
15 es a variety of reflexes including cough and bronchoconstriction.
16 d to the increase in respiratory work during bronchoconstriction.
17 halational anesthetics because of refractory bronchoconstriction.
18 ch is the acute compressive stress caused by bronchoconstriction.
19 2 antagonists may be useful drugs to prevent bronchoconstriction.
20 est a novel pathway by which AQP5 influences bronchoconstriction.
21 ion of M1 and M3 muscarinic receptors causes bronchoconstriction.
22 )-agonists are widely used for the relief of bronchoconstriction.
23 ypercapnia only during moderate, not severe, bronchoconstriction.
24 provides protection against exercise-induced bronchoconstriction.
25 a) and pH 6.87+/-0.11) developed with severe bronchoconstriction.
26 termine whether activation of RARs can cause bronchoconstriction.
27 Hypertonic saline (HTS) induces bronchoconstriction.
28 n-induced changes in ASF osmolality initiate bronchoconstriction.
29 ells, leading to lethal vascular leakage and bronchoconstriction.
30 nts can cause dyspnoea, chest discomfort and bronchoconstriction.
31 tion, and inhibit antigen-induced late-phase bronchoconstriction.
32 ed nitric oxide (FENO) levels decrease after bronchoconstriction.
33 vivo efficacy reducing early and late phase bronchoconstriction.
34 infections increase vagally mediated reflex bronchoconstriction.
35 otect such patients against exercise-induced bronchoconstriction.
36 ation, plasma leakage, leukocyte influx, and bronchoconstriction.
37 es in the lung, potentiating vagally induced bronchoconstriction.
38 tion (DI) to total lung capacity may lead to bronchoconstriction.
39 asthmatic subjects to monitor for excessive bronchoconstriction.
40 kg) and 82% (5 mg/kg) inhibition of allergic bronchoconstriction.
41 g dose of zafirlukast attenuated SO2-induced bronchoconstriction.
42 ient mice, with evident vascular leakage and bronchoconstriction.
43 h or 3 wk BAL, but did not affect the acute bronchoconstriction.
44 docaine at blocking histamine-induced reflex bronchoconstriction.
45 administered to prevent this reflex-induced bronchoconstriction.
46 of acetylcholine, inhibiting vagally induced bronchoconstriction.
47 d intravenous lidocaine block reflex-induced bronchoconstriction.
48 66, however, did not block histamine-induced bronchoconstriction.
49 rapeutic serum concentrations blocked reflex bronchoconstriction.
50 pilocarpine's inhibition of vagally induced bronchoconstriction.
51 ogical RhoA-dependent Ca(2+) sensitivity and bronchoconstriction.
52 Lung nociceptors initiate cough and bronchoconstriction.
53 rin induce IL-33-dependent MC activation and bronchoconstriction.
54 n patients with congestive heart failure and bronchoconstriction.
55 al response to beta(2) agonists resulting in bronchoconstriction.
56 and control of asthma symptoms by reversing bronchoconstriction.
57 s been suggested as a potential modulator of bronchoconstriction.
58 y included 13 patients with exercise-induced bronchoconstriction.
59 er studies of patients with exercise-induced bronchoconstriction.
60 eshold concentrations of allergen to produce bronchoconstriction.
61 duced airway inflammation, eosinophilia, and bronchoconstriction.
62 ves, which upon activation can elicit reflex bronchoconstriction.
63 inspirations are less effective in reversing bronchoconstriction.
64 esponse to histamine, without inhibiting the bronchoconstriction.
65 cetylcholine release and potentiating reflex bronchoconstriction.
66 l activity of nodose C-fibres in response to bronchoconstriction.
67 24 h duration of action in a mouse model of bronchoconstriction.
68 though inhaled iloprost occasionally induced bronchoconstriction.
69 ted heparins attenuate antigen-induced acute bronchoconstriction, (2) nonanticoagulant fractions medi
71 asthma frequently have only exercise-induced bronchoconstriction, a symptom of inadequate control of
73 ave demonstrated that normal infants exhibit bronchoconstriction after inhalation of nonspecific agon
74 ve cigarette smoke) have more wheeze, cough, bronchoconstriction, airway hyper-reactivity and mucous
75 n of heparin (LA-heparin) on antigen-induced bronchoconstriction, airway hyperresponsiveness (AHR), a
76 responses in human airways in vivo, such as bronchoconstriction, airway hyperresponsiveness and infl
77 ma, including bronchial hyperresponsiveness, bronchoconstriction, airway inflammation, and airway rem
78 ing, nasal congestion, rhinorrhea, coughing, bronchoconstriction, airway mucus secretion, dysphagia,
79 late central and local reflex events such as bronchoconstriction, airway plasma leakage, mucus secret
80 us area of high tracer retention (TR) during bronchoconstriction and a second one covering an area of
81 reduction in regional Q to the TR ROI during bronchoconstriction and a variable and nonsignificant ch
82 ympathetic signaling leads to hyperactivated bronchoconstriction and abnormal respiration in the KO n
83 ficacy against exercise and allergen-induced bronchoconstriction and additive benefit for use in pati
84 nificantly blocks antigen-induced late-phase bronchoconstriction and airway hyper-responsiveness in s
85 gest tryptase involvement in both late-phase bronchoconstriction and airway hyperreactivity and furth
86 esults indicate that inhaled tryptase causes bronchoconstriction and airway hyperresponsiveness in al
87 y of airway disease, plays a central role in bronchoconstriction and airway remodeling, including air
88 he synthesis of leukotrienes which can cause bronchoconstriction and airways edema and appear to be i
89 lective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sensitive individuals.
91 eive the same quality of dyspnea during mild bronchoconstriction and external resistive loads, we stu
92 rasympathetic nerves causes vagally mediated bronchoconstriction and hyperresponsiveness following an
93 atment with AMG 157 reduced allergen-induced bronchoconstriction and indexes of airway inflammation b
94 mast cells has been implicated in the severe bronchoconstriction and inflammation prevalent in these
95 Inhaled heparin prevents antigen-induced bronchoconstriction and inhibits anti-IgE-mediated mast-
96 LT receptor or 5-lipoxygenase, implying that bronchoconstriction and MC activation were both cysLT de
98 e certain mechanisms to specific patterns of bronchoconstriction and subsequently match phenotypes of
99 strically), significantly inhibited both the bronchoconstriction and the eosinophilia at 24 h, wherea
101 A(3) adenosine receptor to adenosine-induced bronchoconstriction and to assess the contribution of ma
102 etermine: (1) if aerosolized tryptase causes bronchoconstriction, and (2) the mechanism by which this
103 dose-dependent inhibition of antigen-induced bronchoconstriction, and a 5-mg/kg nebulized dose caused
104 y chronic pulmonary inflammation, reversible bronchoconstriction, and airway hyperreactivity to provo
108 tion and in AHR, but no changes in immediate bronchoconstriction as compared with control recipients.
109 ivation of parasympathetic signaling-induced bronchoconstriction, as evidenced by increased pulmonary
110 herapy for the treatment of inflammation and bronchoconstriction associated with persistent asthma is
112 dose of salmeterol attenuated the degree of bronchoconstriction at all times (decrease in FEV1 on da
113 ed consistent inhibition of exercise-induced bronchoconstriction at the end of the 8-week dosing inte
115 ral infections may increase vagally mediated bronchoconstriction both by directly inhibiting M2 recep
116 mographic lung imaging at baseline and after bronchoconstriction, breathing either room air or 80% ox
117 ge in serum recipients resulted in immediate bronchoconstriction but had no effect on AHR or on pulmo
118 ng and deep inspirations potently antagonize bronchoconstriction, but in the asthmatic lung this salu
119 this response, the antagonism of SO2-induced bronchoconstriction by a single oral dose of the leukotr
121 t chymase protects against cytokine-enhanced bronchoconstriction by cleaving fibronectin to impair te
122 lume was increased equally in the absence of bronchoconstriction by increasing end-expiratory pressur
123 demonstrate that IL-33 exacerbates allergic bronchoconstriction by increasing synthesis, storage, an
127 airway smooth muscle also appear to mediate bronchoconstriction caused by the muscarinic receptor ag
128 onses that influence cardiorenal, pulmonary (bronchoconstriction), central nervous system (locomotion
129 during 92% of the 26 trials of methacholine bronchoconstriction compared with 3% of the 72 trials of
130 e ablation of sensory neurons does not limit bronchoconstriction, constriction after Ag challenge is
131 he airway wall into a rosette pattern during bronchoconstriction creates a complex stress field, with
134 the postbronchodilator baseline ("excessive bronchoconstriction") during their first sputum inductio
135 the treatment of choice for exercise-induced bronchoconstriction (EIB) and act through specific recep
140 methacholine challenge and exercise-induced bronchoconstriction (EIB) test (n = 478) at 10 years and
147 reactivity, whereas WT mice developed marked bronchoconstriction following aerosol Ag sensitization a
148 Thus, in the mouse the initial period of bronchoconstriction following allergen exposure may invo
149 if heparin inhibits hyperventilation-induced bronchoconstriction (HIB) in a canine model of EIA, and
150 activity modulates hyperventilation-induced bronchoconstriction (HIB) in canine peripheral airways a
152 Our findings show that HA blocks PPE-induced bronchoconstriction in a dose-dependent and molecular we
155 rograms albuterol does not prevent excessive bronchoconstriction in all asthmatic subjects undergoing
157 ptor (beta2-AR)-agonists are used to relieve bronchoconstriction in asthma, but may reduce asthma con
158 led beta-agonists are effective at reversing bronchoconstriction in asthma, but the mechanism by whic
159 scle (ASM)-relaxing agents that help reverse bronchoconstriction in asthma, but their ability to affe
162 with des-Arg10-lysylbradykinin did not cause bronchoconstriction in asthmatic subjects or increase gl
165 gonist pilocarpine inhibited vagally-induced bronchoconstriction in control but not challenged animal
167 aintained for a prolonged period after acute bronchoconstriction in humans in the absence of deep ins
168 ene receptor (CysLT(1)R) are efficacious for bronchoconstriction in humans with bronchial asthma; how
170 ETS increases citric acid-induced cough and bronchoconstriction in part by an NK-1 receptor mechanis
172 ntilation of hot humid air induces transient bronchoconstriction in patients with asthma; the underly
173 offsets non-selective beta blockade-induced bronchoconstriction in patients with obstructive airway
174 , activation of airway mast cells (MCs), and bronchoconstriction in response to nonselective cyclooxy
175 led porcine pancreatic elastase (PPE) causes bronchoconstriction in sheep via a bradykinin-mediated m
176 ously shown that heparin attenuates allergic bronchoconstriction in sheep, inhibits anti-IgE mediated
178 by 99%, at an oral dose of 10 mg/kg, and the bronchoconstriction in the allergic guinea pig by 50%, a
179 hallenge evoked a significantly more intense bronchoconstriction in the Ova-sensitized group (control
180 aproxen, diclofenac, or ibuprofen) increased bronchoconstriction in tissue from wild-type but not fro
181 ry activity and long duration of action in a bronchoconstriction in vivo model in mice via intranasal
182 tory activity and long duration of action in bronchoconstriction in vivo models in two species via in
183 osure enhances citric acid-induced cough and bronchoconstriction in young guinea pigs via a neurokini
184 e high levels of IgE antibody and experience bronchoconstriction, increased airway hyperresponsivenes
187 nto murine airways abrogated the exaggerated bronchoconstriction induced by allergen sensitization an
188 d short-term prophylactic protection against bronchoconstriction induced by exercise or other stimuli
190 was designed to test the hypothesis that the bronchoconstriction induced by increasing airway tempera
191 P2X2/3 purinoceptor antagonists, blocked the bronchoconstriction-induced nodose C-fibre discharge.
197 view, we show herein that mast cell-mediated bronchoconstriction is observed only in animals with int
201 Here we present experimental evidence that bronchoconstriction leads to patchiness in lung ventilat
202 room air and 80% O2 conditions (baseline vs. bronchoconstriction, mean +/- SD, 1.02 +/- 0.20 vs. 0.35
203 f ventilation-perfusion (VA/Q) ratios during bronchoconstriction measured with the multiple inert gas
204 , released from activated mast cells, causes bronchoconstriction mediated by H(1) receptors, whereas
205 and pH 7.28+/-0.02) developed with moderate bronchoconstriction; more profound respiratory acidosis
206 are important mediators of asthma by causing bronchoconstriction, mucous secretion, and increased vas
207 sLTs) are potent lipid mediators involved in bronchoconstriction, mucus secretion, and cell trafficki
208 ntilated sheep before and after methacholine bronchoconstriction (n = 3) and pulmonary embolism (n =
209 e by Ascaris suum) abolished both late-phase bronchoconstriction (no significant increase in specific
212 occurred in the healthy subjects but further bronchoconstriction occurred in the subjects with asthma
213 at PAR2 agonists, including tryptase, induce bronchoconstriction of human airway by stimulating smoot
214 l and nonpharmaceutical) of exercise-induced bronchoconstriction or exercise-induced asthma (which is
215 often characterized by an initial period of bronchoconstriction, or early phase reaction (EPR), that
216 s characterized by airway epithelial damage, bronchoconstriction, parenchymal destruction and mucus h
218 P released within the tissues in response to bronchoconstriction plays a pivotal role in the mechanic
221 gs inhibit LTD4-, LTE4-, and antigen-induced bronchoconstriction, reduce inflammatory markers in mode
222 that the bimodality of VA/Q distributions in bronchoconstriction reflects the involvement of large co
224 20 to -69%); no subject developed refractory bronchoconstriction requiring hospitalization or emergen
225 eatment, and no subject developed refractory bronchoconstriction requiring treatment other than rever
226 nists, PGE2 inhibited the mast cell-mediated bronchoconstriction resulting from anti-IgE challenge.
227 y defense responses such as cough and reflex bronchoconstriction, resulting from activation of vagal
228 y and expression of a mediator of endogenous bronchoconstriction, S-nitrosoglutathione (GSNO) reducta
229 ough the measurement of airway inflammation, bronchoconstriction, serum IgE levels, and bronchoalveol
230 d suggest that both ISH and allergen-induced bronchoconstriction share pathobiologic mechanisms that
231 ay be an additional mechanism for decreasing bronchoconstriction, since it would decrease eosinophil
233 greater protection against exercise-induced bronchoconstriction than placebo therapy (expressed as t
234 way, and kallikrein, which mediates allergic bronchoconstriction that limits the inhalation of noxiou
235 primary question is how they are related to bronchoconstriction, the main clinical feature of asthma
236 rienes (cysLTs) mediate vascular leakage and bronchoconstriction through the smooth muscle-associated
237 people worldwide, is defined by exaggerated bronchoconstriction to inflammatory mediators including
238 nificantly increased concentration-dependent bronchoconstriction to intravenously administered Ach, a
239 al stress similar to that experienced during bronchoconstriction triggers epithelial cell signaling t
240 of the reduction in relative perfusion after bronchoconstriction under 80% O2 conditions occurred as
241 w region, relative perfusion decreased after bronchoconstriction under room air conditions and also,
244 n combination with immunohistochemistry, and bronchoconstriction was assessed by whole body plethysmo
250 e prebronchodilator FEV1 > 80% had excessive bronchoconstriction, whereas 10 of the 24 subjects (42%)
251 zed dose caused a 67% inhibition of allergic bronchoconstriction, whereas a 2.5-mg/kg dose was ineffe
253 rways of asthmatic individuals causes severe bronchoconstriction, which is in part neurally mediated
254 neural control of the airways contribute to bronchoconstriction, which is reflected in an increased
255 ors by gallamine potentiated vagally induced bronchoconstriction, while in challenged animals this ef
256 ized guinea pigs, 47.Na dosed orally blocked bronchoconstriction with an ED(50) = 0.4 mg/kg, the most
257 ly to be far more common than is symptomatic bronchoconstriction with beta(2) agonists, but no system
259 main components of asthma (inflammation and bronchoconstriction) with fluticasone propionate and sal
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