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

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

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

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

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

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

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

11 These neurons fire in synchronization with inspiratory activity.

12 recurrent central apnoeas and prolonged post-inspiratory activity.

13 lternating breaths, and responses in maximal inspiratory airflow (V(I)max) and inspiratory airflow li

14 in maximal inspiratory airflow (V(I)max) and inspiratory airflow limitation (IFL) were assessed.

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

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

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

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 These values were measured during 15-sec end-inspiratory and end-expiratory ventilatory occlusions pe

21 inspiratory pattern as well as coordinating inspiratory and expiratory activity.

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

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

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

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

26 Inspiratory and expiratory flows and hemodynamics were m

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 nal area measurements were obtained from end-inspiratory and forced-expiratory CT images for the righ

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

33 Cs) in cat respiratory motoneurones (phrenic inspiratory and thoracic expiratory) was investigated by

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

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

36 spiratory phase-spanning cells, resulting in inspiratory apneusis.

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

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

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

40 Thoracic MR/PET with inspiratory breath-hold MR showed the largest misalignme

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

42 ssed in distinct populations of pre-BotC and inspiratory bulbospinal ventral respiratory group (ibsVR

43 We probed mechanisms underlying inspiratory burst generation in the preBotC using hologr

44 To explore mechanisms relating inspiratory burst generation to rhythmogenesis, we compa

45 activated inward current that contributes to inspiratory burst generation.

46 ratory cycle and discharge greater magnitude inspiratory bursts compared with Dbx1(-) neurons.

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

48 Here, inspiratory bursts were almost always present.

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

50 itic Ca(2+) accumulation frequently precedes inspiratory bursts, particularly at recording sites 50-3

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

52 tory muscle function (P=0.005) and decreased inspiratory capacity (IC; P=0.001).

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 growth and differentiation: vital capacity, inspiratory capacity, compliance, non-parenchymal lung v

56 Dyspnea intensity, inspiratory capacity, oxygen saturation, and cardiac, me

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

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

59 tory valvular-to-annular ratio (P=0.026) and inspiratory change in right ventricular length-to-width

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

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

62 a preBotC burst occurred, its high amplitude inspiratory component (I-burst) was preceded by a preins

63 End-expiratory and end-inspiratory computed tomography scans were performed at

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

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

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

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

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

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

70 rtension (PH) causes loss of body weight and inspiratory (diaphragm) muscle dysfunction.

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

72 arge was nearly abolished, whereas laryngeal inspiratory discharge was increased disproportionally.

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

74 g pathway in XII motoneurones that modulates inspiratory drive currents and plasticity of XII motoneu

75 lated rhythm, hypoglossal (XII) motoneuronal inspiratory drive currents and respiratory-related XII n

76 dual capacity for potentiating AMPA-mediated inspiratory drive to XII MNs that might be applied to th

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

78 in SNA are not dependent upon stimulation of inspiratory drive.

79 y peptide to PKG (PKGI) increased endogenous inspiratory-drive currents and exogenous AMPA-induced cu

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

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

82 he results show that, per unit pressure, the inspiratory effect of the diaphragmatic force on the low

83 he insertional force contributes 60% of that inspiratory effect.

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

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

86 ed in large decrement, approximately 96%, in inspiratory effort compared with spontaneously breathing

87 index was also used to measure the patient's inspiratory effort from Eadi without esophageal pressure

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

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

90 The inspiratory effort measured by the esophageal pressure t

91 Furthermore, although no inspiratory effort occurs during controlled mechanical v

92 ever, variable pressure support yielded less inspiratory effort than proportional assist ventilation

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

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

95 n enables a continuous estimate of patient's inspiratory effort.

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

97 e of 0 cm H2O and the other targeting an end-inspiratory elastance-based transpulmonary pressure of 2

98 e of 0 cm H2O and the other targeting an end-inspiratory elastance-based transpulmonary pressure of 2

99 ry pressure of 0 cm H2O and targeting an end-inspiratory elastance-based transpulmonary pressure of 2

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

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

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

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

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

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

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

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

116 e were associated with increases in VI, mean inspiratory flow (Vt/Ti) and tonic and phasic components

117 , duty cycle >0.41 increased mean expiratory-inspiratory flow bias from -4.1 +/- 4.6 to 7.9 +/- 5.9 L

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

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

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

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

122 athing frequency, due primarily to decreased inspiratory flow rate.

123 toms scores, nasal secretions and peak nasal inspiratory flow were measured.

124 ric oxide (FeNO), smell test, and peak nasal inspiratory flow were used.

125 ts normalized Penh values and increased peak inspiratory flow, leading to decreased inspiration times

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

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

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

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

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

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

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

133 ut, stroke volume variation and, with use of inspiratory hold maneuvers, mean systemic filling pressu

134 Inspiratory holds were performed at baseline-1, during i

135 so with axon collaterals to areas containing inspiratory hypoglossal (XII) premotoneurons and motoneu

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

137 by active compression-decompression CPR, an inspiratory impedance threshold device (ITD), and abdomi

138 but the lung inflation-induced Breuer-Hering inspiratory inhibitory reflex was suppressed.

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

140 To assess these forces, the inspiratory intercostal muscles in all interspaces were

141 Most commissural pre-BotC inspiratory interneurons were glutamatergic, with a subs

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

143 Active inspiratory laryngeal narrowing during nasal pressure su

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

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

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

147 cle and ventilatory pump), during Ex plus an inspiratory load of 12.8 +/- 1.5 cm water, and during Ex

148 30 healthy subjects performed two identical inspiratory loading tasks.

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

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

151 In health, peak Vt and end-inspiratory lung volume increased significantly with DS.

152 This population of inspiratory-modulated GABAergic neurons could also play

153 nclude that there is a population of preBotC inspiratory-modulated glycinergic, presumably inhibitory

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

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

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

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

158 preBotC) produces rhythmic bursts that drive inspiratory motor output.

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

160 opulation-wide bursts of activity to control inspiratory movements.

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

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

163 essments included exercise duration, surface inspiratory muscle EMG, Spo(2), transcutaneous Pco(2), a

164 S may provide a more physiological method of inspiratory muscle pacing.

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

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

167 ous methods of electrical stimulation of the inspiratory muscles, high frequency spinal cord stimulat

168 les is less well understood than that of the inspiratory muscles, particularly in the rat.

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

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

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

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

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

174 tion if they acted primarily to inhibit post-inspiratory neurons and thereby release inspiration neur

175 ablished by single-cell RT-PCR that pre-BotC inspiratory neurons express TASK-1 and in some cases als

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

177 The amplitude of evoked EPSPs was smaller in inspiratory neurons from alpha(1A)(-)/(-) mice compared

178 Conotoxin GVIA abolished all EPSPs in inspiratory neurons from alpha(1A)(-)/(-) mice, while th

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

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

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

182 itude and frequency of intrinsic bursting in inspiratory neurons.

183 -cell subtractive cDNA library from pre-BotC inspiratory neurons.

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

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

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

187 % +/- 1%, respectively; p < 0.0001), and end-inspiratory occlusion decreased velocity-time integral m

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

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

190 tation (iPMF), a rebound increase in phrenic inspiratory output observed once respiratory neural driv

191 (2) inactivity-induced increases in phrenic inspiratory output require local PKCzeta/iota activity t

192 This may prevent injury from inspiratory overdistention and expiratory alveolar colla

193 Control animals were maintained on an inspiratory oxygen fraction of 0.4.

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

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

196 le of pre-BotC inhibitory neurons in shaping inspiratory pattern as well as coordinating inspiratory

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 Nasal inspiratory peak flow monitoring was less sensitive to o

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

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

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

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

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

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

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

208 lateral PAG converted the pre-I neurons into inspiratory phase-spanning cells, resulting in inspirato

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 Assignment of signals to alveolar or inspiratory phases was done automatically by a matlab-ba

214 1B); low tidal volume (1A) and limitation of inspiratory plateau pressure (1B) for acute respiratory

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

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

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

218 115 (83%) of these patients had not received inspiratory positive pressure ventilation (IPPV) despite

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 reduced capacity of the diaphragm to produce inspiratory pressure (diaphragm dysfunction) is frequent

223 m, and manuvacuometric measurements [maximal inspiratory pressure (MIP) and maximal expiratory pressu

224 24 hrs later by mechanical ventilation (peak inspiratory pressure 22 cm H(2)O and positive end-expira

225 tive end-expiratory pressure 15 cm H2O, peak inspiratory pressure 35-40 cm H2O for 30 secs, group RM)

226 Peak inspiratory pressure and diaphragm electrical activity w

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

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

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

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

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

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

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

234 Inspiratory pressure was adjusted to control tidal volum

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

236 Peak inspiratory pressure, positive end-expiratory pressure,

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

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

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

240 (4-8 ml/kg predicted body weight) and lower inspiratory pressures (plateau pressure < 30 cm H2O) (mo

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

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

243 and bilaterally synchronized contractions of inspiratory pump muscles.

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

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

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

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

248 ex assemble excitatory networks that produce inspiratory-related neural rhythms, but the importance o

249 Breathing in mammals depends on an inspiratory-related rhythm that is generated by glutamat

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

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

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

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

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

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

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

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

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

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

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

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

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

263 (preBotC) as the site for the generation of inspiratory rhythm and (b) the retrotrapezoid nucleus/pa

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

265 s (RTN) neurons results in severely impaired inspiratory rhythm and pronounced neonatal death.

266 esis that the preBotzinger complex generates inspiratory rhythm and the retrotrapezoid nucleus-parafa

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

268 complex (pre-BotC), the structure generating inspiratory rhythm in the brainstem.

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

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

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

272 /4, and 20/4 cm H2O), using a broad range of inspiratory rise times from 0.05 to 0.4 s.

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

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

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

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

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

278 t girl presenting with an encephalomyopathy, inspiratory stridor, ventilator failure, progressive hyp

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

280 Inspiratory thoracic pressure reduction is expected to d

281 t respiratory depression combining increased inspiratory (TI) and expiratory times (TE).

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

283 Inspiratory time in excess was shorter in neurally adjus

284 ity, leak volume, inspiratory trigger delay, inspiratory time in excess, and the five main asynchroni

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

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

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

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

289 In this model, the end-inspiratory transpulmonary open lung approach minimized

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

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

292 ranspulmonary pressure but did not alter end-inspiratory transpulmonary pressure.

293 Inspiratory trigger delay was not affected by the noninv

294 diaphragm electrical activity, leak volume, inspiratory trigger delay, inspiratory time in excess, a

295 inspiration was independently determined by inspiratory valvular-to-annular ratio (P=0.026) and insp

296 1 second (FEV1) and FEV1 as a percentage of inspiratory vital capacity (FEV1%VC) were assessed with

297 icient mice restores alveologenesis and lung inspiratory volume and compliance function.

298 presence or absence of posttussive emesis or inspiratory whoop modestly change the likelihood of pert

299 conditions where periods between successive inspiratory XII bursts were highly variable and distribu

300 ted ipsilaterally also to regions containing inspiratory XII premotoneurons and motoneurons, whereas