ライフサイエンスコーパス: inspiratory

1 The diaphragm has an inspiratory action on the lower ribs, and current conven

2 The normal diaphragm has an inspiratory action on the lower ribs, but subjects with

3 Hyperpolarizing preBotC neurons decreased inspiratory activity and initiated active expiration, ul

4 nic MNs integrate multiple inputs to mediate inspiratory activity during breathing and are constraine

5 o effect on breathing at rest, or changes in inspiratory activity induced by hypoxia and hypercapnia;

6 e rise times tested did not alter the phasic inspiratory activity of glottal constrictor muscle durin

7 Finally, no alterations in the phasic inspiratory activity of glottal constrictor muscle durin

8 percentage of respiratory cycles with phasic inspiratory activity of glottal constrictor muscle was m

9 ut in vivo and in incomplete transmission of inspiratory activity to the hypoglossus motor nucleus.

10 uced active expiration at rest, but not when inspiratory activity was suppressed by hyperpolarizing p

11 hypoxia- and hypercapnia-induced increase in inspiratory activity, and when present, reducing expirat

12 recurrent central apnoeas and prolonged post-inspiratory activity.

13 activate chemosensitive neurons and increase inspiratory activity.

14 broader set of multiscale variables, such as inspiratory airway dimension, expiratory air trapping, a

15 wall and that compensation for more negative inspiratory airway pressures generated during heavy exer

16 Mean end-inspiratory and end-expiratory arterial pressures at t =

17 The inspiratory and end-expiratory cross-sectional areas of

18 ynamics was analyzed beat-to-beat in the end-inspiratory and end-expiratory cycle comparing the IPPV

19 anspulmonary pressure difference between end-inspiratory and end-expiratory pauses.

20 duals had undergone limited (three-location) inspiratory and end-expiratory thoracic CT before and af

21 ow measurements are not corrected for phasic inspiratory and expiratory changes in clinical practice.

22 Subjects underwent inspiratory and expiratory chest CT and spirometry at ba

23 We analyzed 8,034 subjects with complete inspiratory and expiratory computed tomographic data par

24 nical questionnaires, spirometry, volumetric inspiratory and expiratory computed tomography, and long

25 terquartile range, 0.4-0.53) yielding a mean inspiratory and expiratory concentrations of 0.79% (SD,

26 response mapping (PRM), a technique pairing inspiratory and expiratory CT images to define emphysema

27 By matching inspiratory and expiratory images voxel by voxel using i

28 e of ventilation per lobe from the change in inspiratory and expiratory lobar volumes.

29 rhythmic oscillations generated by brainstem inspiratory and expiratory neurons.

30 trapping, airway size, and lung volume with inspiratory and expiratory X-ray computed tomography sca

31 es, it is reasonable to assume that negative inspiratory and positive expiratory intrathoracic pressu

32 Lower V(RM) predicted high end-inspiratory and tidal lung stress (end-inspiratory: beta

33 ained independently associated with both end-inspiratory and tidal stress.

34 CT scores assessed at baseline, quantitative inspiratory, and expiratory CT and at 5 years.

35 al recruitment of muscles in the expiratory, inspiratory, and postinspiratory (post-I) phases of the

36 red with PEEP of 16 cm H2O (mean [SEM] total inspiratory area, 52.0% [2.9%] vs 29.4% [4.3%], respecti

37 emotor excitatory drive, contributing to the inspiratory behavior of XII motoneurons, as well as a ke

38 h end-inspiratory and tidal lung stress (end-inspiratory: beta = -0.449; 95% CI, -0.664 to -0.234; p

39 ing an interoceptive perturbation condition (inspiratory breath-holding during heartbeat tapping), he

40 Using a cued inspiratory breathing load paradigm, we compared women r

41 ing an (1) emotion face-processing task, (2) inspiratory breathing load task, and (3) fear conditioni

42 ex (preBotC) generates the rhythm underlying inspiratory breathing movements and its core interneuron

43 Inspiratory breathing movements depend on pre-Botzinger

44 tidal recruitment/derecruitment, mechanical inspiratory breaths redistributed blood volume away from

45 phrenic nerve stimulation on user-specified inspiratory breaths while on mechanical ventilation.

46 Under rhythmic conditions, in each cycle, an inspiratory burst emerges as (presumptive) preBotC rhyth

47 t features of preBotC network dynamics where inspiratory bursts arise when and only when the preBotC

48 period ( approximately 2 s) after endogenous inspiratory bursts that precludes light-evoked bursts in

49 piration (for ~50-500 ms), which can trigger inspiratory bursts that propagate to motoneurons.

50 synaptic excitation is required to initiate inspiratory bursts, but whether excitatory synaptic mech

51 eBotC population activity consists of strong inspiratory bursts, which drive motoneuronal activity, a

52 cycle period nor the magnitude of endogenous inspiratory bursts-is sensitive to changes in extracellu

53 sociation of Th1/Th2 ratio with RV, FRC, and inspiratory capacity was attenuated after adjusting for

54 n of activity, slightly lower FEV1, FVC, and inspiratory capacity, and greater airway-wall thickening

55 lation (assessed by changes from baseline in inspiratory capacity, DeltaIC) was less during IE than C

56 moderate ILD or COPD with similarly reduced inspiratory capacity, the peak oxygen uptake, work rate,

57 Completely absent in spinal inspiratory cells, this rhythmic pattern is highly corre

58 -2017 with postbronchodilator spirometry and inspiratory chest CT to quantify percent emphysema.

59 This work reveals the existence of a core inspiratory circuit in which V0 to V0 synapses enabling

60 eurons, which are a crucial component of the inspiratory circuit.

61 e evaluated the results of paired expiratory/inspiratory computed tomography in a cohort of asthmatic

62 atment was 55.6 +/- 2.5 (SD) min at a median inspiratory concentration of 44% (interquartile range, 3

63 th hypocapnia, however, had worse mechanical inspiratory constraints and higher dyspnea scores for a

64 o that observed during volitional breathing, inspiratory constraints, or in patients with defective a

65 : Participants underwent post-bronchodilator inspiratory CT, and prebronchodilator and post-bronchodi

66 m-selective positive end-expiratory pressure-inspiratory-CT (2.8 +/- 1.1 vs 0.6 +/- 0.3; p = 0.01); a

67 imum global positive end-expiratory pressure-inspiratory-CT and optimum-selective positive end-expira

68 ifference between end-expiratory and minimum-inspiratory diameter over the end-expiratory diameter.

69 In ILD and COPD, descriptors alluding to inspiratory difficulty were selected more frequently, wi

70 we found that, during central apnoeas, post-inspiratory drive (adductor motor) to the upper airways

71 ow amplitude inspiration due to loss of post-inspiratory drive) that was rapidly reversed by the opio

72 ory frequency, IRt inhibition did not affect inspiratory duration or abolish the recruitment of post-

73 tion increased tidal volume without altering inspiratory duration, whereas expiratory-phase photoinhi

74 ry-modulated with peak discharge in the late inspiratory/early expiratory phase and this activity was

75 cure bilaterally coordinated contractions of inspiratory effector muscles required for efficient brea

76 9] vs. 138 [101-172]; P = 0.001) and lowered inspiratory effort (7 cm H(2)O [4-11] vs. 15 [8-19]; P =

77 ctive studies incorporating the magnitude of inspiratory effort and adjusting for all potential sever

78 multiple physiologic effects including less inspiratory effort and improved lung volume and complian

79 ort reduction by NIV was linearly related to inspiratory effort during HFNC (r = 0.84; P < 0.001).

80 dition, because the lack of reliable data on inspiratory effort in our study, prospective studies inc

81 ilatory support to maintain normal levels of inspiratory effort may prevent changes in diaphragm conf

82 pulmonary vascular pressure swings caused by inspiratory effort may worsen vascular leakage.

83 The inspiratory effort measured by the esophageal pressure t

84 e.Objectives: To explore the hypothesis that inspiratory effort might be a major determinant of NIV f

85 9]; P = 0.11), but patients exhibiting lower inspiratory effort on HFNC experienced increases in tran

86 Inspiratory effort reduction by NIV was linearly related

87 Rationale: The role of inspiratory effort still has to be determined as a poten

88 Inspiratory effort was estimated by esophageal pressure

89 t NIV improves oxygenation, reduces dyspnea, inspiratory effort, and simplified pressure-time product

90 ach phase, we measured arterial blood gases, inspiratory effort, and work of breathing by esophageal

91 assess the effects of HFNC on gas exchange, inspiratory effort, minute ventilation, end-expiratory l

92 atory drive and detect potentially injurious inspiratory effort.

93 es the control of V. e almost exclusively to inspiratory effort.

94 tio of change in Pes to change in Paw during inspiratory efforts against a closed airway.

95 In such cases, when assist is high, weak inspiratory efforts promote ineffective triggering, peri

96 tical component with subsequent reduction of inspiratory endurance by half.

97 CON, n = 7) during pulmonary function tests, inspiratory endurance testing, dynamic kinematic MRI of

98 or output and inspiratory endurance.Methods: Inspiratory endurance was investigated twice in random o

99 deprivation on respiratory motor output and inspiratory endurance.Methods: Inspiratory endurance was

100 We analyzed paired inspiratory-expiratory computed tomography images at bas

101 Analysis of paired inspiratory-expiratory computed tomography images from a

102 ssion in Dbx1 preBotC neurons influences the inspiratory-expiratory phase transition during respirato

103 atory synaptic mechanisms also contribute to inspiratory-expiratory phase transition is unknown.

104 he role of short-term synaptic depression in inspiratory-expiratory phase transition.

105 rametric response mapping analysis of paired inspiratory/expiratory CTs to identify functional small

106 and regulates respiration, in particular the inspiratory/expiratory phase transition.

107 ay pressure release ventilation mode with an inspiratory/expiratory ratio of 1:1.

108 e, 6 mL/kg; respiratory rate, 40; FIO2, 0.6; inspiratory:expiratory, 1:2; and positive end-expiratory

109 onsive preBotC neurons had preinspiratory or inspiratory firing patterns associated with excitatory e

110 There was a fall in peak nasal inspiratory flow (PNIF) between baseline vs. first dose

111 pecific immunoglobulin levels and peak nasal inspiratory flow (PNIF) were also measured (all measures

112 Nasal symptoms and peak nasal inspiratory flow (PNIF) were recorded along with periphe

113 peak nasal inspiratory flow (PNIF), acoustic rhinometry (AR) and rh

114 as assessed by symptom scores and peak nasal inspiratory flow (PNIF).

115 as assessed by symptom scores and peak nasal inspiratory flow (PNIF).

116 on cohort correlated with drop in peak nasal inspiratory flow (Spearman's r = 0.314, P = 0.034), and

117 significantly higher than the lung sound of inspiratory flow around 1.0L/s due to rest breathing.

118 beta(2) agonist inhalation was clearer at an inspiratory flow around 1.0L/s than that around 2.0L/s.

119 d 99% frequency (F(99)) in the lung sound of inspiratory flow around 2.0L/s due to slightly strong br

120 ry symptoms, the lung sound spectrums of the inspiratory flow before and after inhalation of a beta(2

121 H2O and TITTOT to achieve a mean expiratory-inspiratory flow bias of 10 L/min (treatment); 3) in Tre

122 The mean expiratory-inspiratory flow in the treatment, control, and Trendele

123 UAO was defined by inspiratory flow limitation (measured by RIP and esophag

124 ntilation (VI)(P </= 0.01) and 251% for mean inspiratory flow rate (VT /TI ) (P </= 0.05) when the CB

125 lation, intervocalization interval, and peak inspiratory flow were identified to increase the transla

126 sured total nasal symptom scores, peak nasal inspiratory flow, nasal (0-8 hours) and serum cytokines,

127 y, airflow and resistance, mainly peak nasal inspiratory flow, rhinomanometry and acoustic rhinometry

128 ith total nasal symptom score and peak nasal inspiratory flow.

129 ese patients decreased, and their peak nasal inspiratory flows increased.

130 sal Outcome Test (SNOT20) scores, peak nasal inspiratory flows, Asthma Control Questionnaire scores,

131 here it is thought that excitation increases inspiratory frequency and inhibition causes apnea.

132 e P2Y1 receptor-mediated increase in fictive inspiratory frequency involves Ca(2+) recruitment from i

133 imulation of inhibitory neurons can increase inspiratory frequency via postinhibitory rebound.

134 n of IV agents, sevoflurane was added to the inspiratory gas flow.

135 ed by stimulation of opioid receptors in the inspiratory-generating regions of the brain.

136 ure tidal strain from end-expiratory and end-inspiratory images in six regions of interest.

137 ow amplitude, inspiratory time fraction, and inspiratory inflation contour) and cycling frequency.

138 In the present study, the inspiratory intercostal muscles in all interspaces in an

139 bilateral lead placement demonstrated a mean inspiratory lag for phrenic nerve stimulation of 23.7 ms

140 iously reported the development of an active inspiratory laryngeal narrowing against ventilator insuf

141 Active inspiratory laryngeal narrowing during nasal pressure su

142 sure rise time or a low PaCO2 level promotes inspiratory laryngeal narrowing observed in nasal pressu

143 ther understand the factors involved in this inspiratory laryngeal narrowing.

144 or N2 (PaO2 = 45-55 mm Hg) was added to the inspiratory line.

145 ustments to single-breath inspiratory loads (inspiratory load compensation, ILC).

146 iratory muscle metaboreflex persisted during inspiratory loading performed at equal absolute intensit

147 aphragm is more susceptible to fatigue after inspiratory loading under acute hypoxic conditions.

148 g day during anticipation and application of inspiratory loading using 7 T functional MRI.

149 d a similar pressor response to work-matched inspiratory loading, independent of oxygen availability.

150 iaphragmatic fatigue (DF) after work-matched inspiratory loading.

151 tched for absolute diaphragmatic work during inspiratory loading.

152 and ventilatory adjustments to single-breath inspiratory loads (inspiratory load compensation, ILC).

153 During single-breath inspiratory loads, inspiratory time and airflow accelera

154 The dependent variables were inspiratory lung density at 15th percentile (adjusted fo

155 , the COPD group failed to increase peak end-inspiratory lung volume and had a significantly smaller

156 C1 neurons play a key role in regulating inspiratory modulation of sympathetic activity and arter

157 of V0s results in left-right desynchronized inspiratory motor commands in reduced brain preparations

158 the threshold for apnoea, inactivity-induced inspiratory motor facilitation (iMF) and long-term facil

159 orms of plasticity called inactivity-induced inspiratory motor facilitation (iMF) and long-term facil

160 hythmic preBotC activity sufficient to drive inspiratory motor output or increased chemosensory drive

161 ich are glutamatergic, decreased ipsilateral inspiratory motor output without affecting frequency.

162 ntilatory disorders characterized by reduced inspiratory motor output, such as sleep apnoea, endogeno

163 Prostaglandin E2 (PGE2) augments distinct inspiratory motor patterns, generated within the preBotz

164 r free-breathing MR was more exact than with inspiratory MR.

165 RATIONALE: The diaphragm is the major inspiratory muscle and is assumed to relax during expira

166 -threshold loading (PTL), women have greater inspiratory muscle endurance time, slower rate of diaphr

167 sex differences in diaphragm fatigue and the inspiratory muscle metaboreflex persisted during inspira

168 th blunted cardiovascular consequences (i.e. inspiratory muscle metaboreflex).

169 against mechanical constraints or with weak inspiratory muscle, and in patients with defective medul

170 eads to atrophy and dysfunction of the major inspiratory muscle, the diaphragm, contributing to venti

171 y disease (COPD), increased activity of neck inspiratory muscles has been reported as a compensatory

172 In vitro responses of the preBotC inspiratory network, preBotC inspiratory neurons and cul

173 ey association between dyspnea intensity and inspiratory neural drive to the diaphragm.

174 uring hypoxia and acts via P2Y1 receptors on inspiratory neurons (and/or glia) to evoke Ca(2+) releas

175 of the preBotC inspiratory network, preBotC inspiratory neurons and cultured preBotC glia to puriner

176 ses in intracellular Ca(2+) ([Ca(2+) ]i ) in inspiratory neurons and glia.

177 een described, but little is known regarding inspiratory neurons expressing pacemaker properties at e

178 inger Complex (BotC) and NK1R-immunoreactive/inspiratory neurons in the preBotC.

179 In current clamp recordings obtained from inspiratory neurons of the preBotC, we found an increase

180 ts in whole cell voltage clamp recordings of inspiratory neurons revealed no changes in inhibitory or

181 itude and frequency of intrinsic bursting in inspiratory neurons.

182 d during the last 5 seconds of 15-second end-inspiratory occlusion and end-expiratory occlusion and a

183 If consecutive end-inspiratory occlusion and end-expiratory occlusion chang

184 hageal Doppler induced by two successive end-inspiratory occlusion and end-expiratory occlusion maneu

185 e last 5 seconds of successive 15-second end-inspiratory occlusion and end-expiratory occlusion, sepa

186 tigated whether adding the effects of an end-inspiratory occlusion and of an end-expiratory occlusion

187 3% +/- 1%, respectively; p < 0.0001) and end-inspiratory occlusion decreased cardiac index estimated

188 % +/- 1%, respectively; p < 0.0001), and end-inspiratory occlusion decreased velocity-time integral m

189 A 15-second end-expiratory occlusion and end-inspiratory occlusion, separated by 1 minute, followed b

190 neurons, photoresponsive preBotC neurons had inspiratory or postinspiratory firing patterns associate

191 isms of compensatory plasticity that augment inspiratory output and lower the threshold for apnoea, i

192 c neural apnoeas triggered increased phrenic inspiratory output in rats in which spinal NR2B-containi

193 hypoxia trigger compensatory enhancements in inspiratory output when experienced separately, forms of

194 not mild) hypoxaemia do not elicit increased inspiratory output, suggesting that concurrent induction

195 The respective proportion of the different inspiratory pacemaker subtypes changes during prenatal d

196 de that glycinergic preBotC neurons modulate inspiratory pattern and are important for reflex apneas,

197 laxation (airway pressure drop during an end-inspiratory pause [in cm H2O]).

198 airway minus esophageal) pressure during end-inspiratory pause of a tidal breath and tidal stress as

199 5 and 45 cm H2O during an end-expiratory/end-inspiratory pause to measure lung recruitability.

200 This also abolished the post-inspiratory peak of cardiac vagal discharge (and cyclica

201 hibition did not affect the amplitude of the inspiratory peak, expiratory trough or expiratory peak o

202 pontine Kolliker-Fuse nucleus, removed post-inspiratory peaks in efferent cardiac vagal activity and

203 ion of controlled expiration during the post-inspiratory phase engages a distributed neuronal populat

204 pre-BotC), a medullary region generating the inspiratory phase of breathing in mammals.

205 rk architecture underlying generation of the inspiratory phase of breathing is not static but can be

206 uvacine (50-70 nl, 10 mm) to remove the post-inspiratory phase of respiration.

207 yhthmia (RSA), with maximum tone in the post-inspiratory phase of respiration.

208 al discharge, which continued throughout the inspiratory phase, while at the same time attenuating di

209 ing cycle by selectively shortening the post-inspiratory phase.

210 bursts and synchronizing activity during the inspiratory phase.

211 In ChR2-transfected mice, brief inspiratory-phase bilateral photostimulation targeting t

212 Inspiratory-phase photoinhibition in Arch-transfected mi

213 Individual sighs (2 x 10 s at inspiratory plateau pressure of 30 cm H2O) largely resto

214 Inspiratory plateau pressure was comparable in both grou

215 al-ventilation strategies that use lower end-inspiratory (plateau) airway pressures, lower tidal volu

216 The median home ventilator settings were an inspiratory positive airway pressure of 24 (IQR, 22-26)

217 115 (83%) of these patients had not received inspiratory positive pressure ventilation (IPPV) despite

218 a three-part respiratory cycle composed from inspiratory, postinspiratory (post-I), and late-expirato

219 to substance P, putatively corresponding to inspiratory pre-Botzinger complex (preBotC) neurons.

220 reBotC Dbx1(+) neurons are rhythmogenic, (2) inspiratory preBotC Dbx1(+) and SST(+) neurons primarily

221 ragm muscle in the mouse, that the principal inspiratory premotor neurons share V0 identity with, and

222 Maximal inspiratory pressure (PI(MAX)) reflects inspiratory weak

223 On enrollment, maximum inspiratory pressure (Pi(max)) was 41.3 (95% confidence

224 Both oxygenation and peak inspiratory pressure are associated with mortality in pe

225 Indices of respiratory function (maximum inspiratory pressure generation and the rapid shallow br

226 rowing against ventilator insufflations when inspiratory pressure is increased during nasal pressure

227 on (higher PaO2/FIO2) rather than lower peak inspiratory pressure or DeltaP, as oxygenation was more

228 Peak inspiratory pressure positively correlated with total lu

229 cally, we tested the hypothesis that a short inspiratory pressure rise time or a low PaCO2 level prom

230 The different inspiratory pressure rise times tested did not alter the

231 (n = 145) or NIV delivered via facial mask (inspiratory pressure support level, 5-15 cm H2O; positiv

232 l sleep apnea by delivering servo-controlled inspiratory pressure support on top of expiratory positi

233 Inspiratory pressure was adjusted to control tidal volum

234 Pdi, but the predictive power of sniff nasal inspiratory pressure was also excellent.

235 Peak inspiratory pressure, positive end-expiratory pressure,

236 At 24 hours, peak inspiratory pressure, positive end-expiratory pressure,

237 etermine whether respiratory mechanics (peak inspiratory pressure, positive end-expiratory pressure,

238 fluence of acute hypoxia during work-matched inspiratory pressure-threshold loading (PTL) on DF in he

239 In response to inspiratory pressure-threshold loading (PTL), women have

240 te infusion, cardiac arrest, PaCO2, and peak inspiratory pressure.

241 (4-8 ml/kg predicted body weight) and lower inspiratory pressures (plateau pressure < 30 cm H2O) (mo

242 TT), acute elevation in peak airway and peak inspiratory pressures are noted in conjunction with desa

243 nt increase in peak airway, plateau and peak inspiratory pressures.

244 ow positive end-expiratory pressure and high inspiratory pressures.

245 Following inspiratory PTL, the magnitude of reduction in P(di,tw)

246 and bilaterally synchronized contractions of inspiratory pump muscles.

247 asured based on mean lung density expiratory/inspiratory ratio was greater in patients with severe an

248 asured based on mean lung density expiratory/inspiratory ratio was significantly increased in patient

249 rongly with the mean lung density expiratory/inspiratory ratio, a CT marker of expiratory air trappin

250 ons affected breathing at rest by decreasing inspiratory-related activity, attenuating the hypoxia- a

251 s of their firing frequency and amplitude of inspiratory-related sympathetic activity in rats in norm

252 A Vt inflection and critically reduced inspiratory reserve volume occurred at a lower (P < 0.05

253 atory flow limitation (EFL); (ii) through an inspiratory resistance (RES) of ~5 cmH(2) O L(-1) s(-1)

254 -175) mL/cm H2O at 60 L/min (p = 0.007), and inspiratory resistance decreased from 9.6 (5.5-13.4) to

255 In all DPI, inspiratory resistance increases with the increasing flo

256 means of inspiration of patients themselves, inspiratory resistance of DPI is an important factor for

257 Therefore, we measured inspiratory resistance of DPI of agents for asthma contr

258 ld instruct patients to inhaler DPI based on inspiratory resistance of the DPI.

259 of this study was to determine the effect of inspiratory resistance through an impedance threshold de

260 ham, no resistance) versus an ITD (increased inspiratory resistance) in 26 patients with postural tac

261 ate, minute volume, dynamic lung compliance, inspiratory resistance, and blood gases.

262 CS exposed mice showed significant increased inspiratory resistance, functional residual capacity, ri

263 /min, we read off suction pressures and find inspiratory resistances by calculation (=suction pressur

264 c vagal tone is intrinsically linked to post-inspiratory respiratory control using the unanaesthetize

265 g of Dbx1-derived interneurons that generate inspiratory rhythm and motor pattern.

266 While it is widely accepted that inspiratory rhythm generation depends on the pre-Botzing

267 (preBotC) neurons, which form the kernel for inspiratory rhythm generation, directly modulate cardiov

268 zinger complex (preBotC), a critical site of inspiratory rhythm generation, release a gliotransmitter

269 cytes in the pre-Botzinger Complex (preBotC) inspiratory rhythm-generating network acts via P2Y1 rece

270 We conclude that inspiratory rhythmogenesis is an emergent process, modul

271 If burstlets underlie inspiratory rhythmogenesis, respiratory depressants, suc

272 A paradoxical inspiratory rise in right atrial pressure (in contrast t

273 Kussmaul physiology was defined as inspiratory rise in right atrial pressure during right h

274 /4, and 20/4 cm H2O), using a broad range of inspiratory rise times from 0.05 to 0.4 s.

275 essure support ventilation is not altered by inspiratory rise times ranging from 0.05 to 0.4 s or by

276 ous plugging, or other airway abnormalities (inspiratory scans) and trapped air (expiratory scans).

277 isa syndrome, contractures of hands or feet, inspiratory sighs, severe dysphonia, severe dysarthria,

278 equency inspiratory sounds (HFIS, defined as inspiratory sounds > 2 kHz) while they slept.

279 g while awake) generated loud high frequency inspiratory sounds (HFIS, defined as inspiratory sounds

280 End-inspiratory stress was defined as the transpulmonary (ai

281 Both patients developed inspiratory stridor and acute hypoxemic respiratory fail

282 and contractile activity (quantified by the inspiratory thickening fraction) were measured daily by

283 Inspiratory thoracic pressure reduction is expected to d

284 ssible until task failure against a moderate inspiratory threshold constraint.

285 During single-breath inspiratory loads, inspiratory time and airflow acceleration increased to p

286 ncreased integrated phrenic nerve discharge, inspiratory time and respiratory drive in rats.

287 Inspiratory time and respiratory rate did not improve Vt

288 or pressure increases noncystic lung Vt, but inspiratory time does not correlate with Vt of normal or

289 essure change (influenced by flow amplitude, inspiratory time fraction, and inspiratory inflation con

290 Pressure-support ventilation and increased inspiratory time were independently associated with the

291 lung strain rates (ratio between strain and inspiratory time).

292 Purpose To evaluate elastic registration of inspiratory-to-expiratory lung MRI for the assessment of

293 Conclusion Elastic registration of inspiratory-to-expiratory MRI shows less lung base respi

294 lets ventilated with low strain rates had an inspiratory-to-expiratory time ratio of 1:2-1:3.

295 ilated with high strain rates had much lower inspiratory-to-expiratory time ratios (down to 1:9).

296 ches to setting Vt may include limits on end-inspiratory transpulmonary pressure, lung strain, and dr

297 expiratory lung volumes while decreasing end-inspiratory transpulmonary pressure, suggesting an impro

298 1 second (FEV1) and FEV1 as a percentage of inspiratory vital capacity (FEV1%VC) were assessed with

299 imal inspiratory pressure (PI(MAX)) reflects inspiratory weakness in late-onset Pompe disease (LOPD).

300 agm is protected against severe fatigue when inspiratory work is excessive and as a result does not e