ライフサイエンスコーパス: minute ventilation

1 changes in body temperature, heart rate, and minute ventilation.

2 O2, PaO2, respiratory system compliance, and minute ventilation.

3 SCH, but there was no significant effect on minute ventilation.

4 on (MV) strategies that intentionally reduce minute ventilation.

5 patients with CHF to markedly increase their minute ventilation.

6 to -0.13; I = 84.0%), but not heart rate or minute ventilation.

7 es included compliance, Pao2:Fio2 ratio, and minute ventilation.

8 adjusting the frequency to maintain constant minute ventilation.

9 10 with 15% arteriovenous shunt and baseline minute ventilation.

10 n oxygen delivery, under conditions of fixed minute ventilation.

11 4.3 to 1.3 hours; P = .36), daily changes of minute-ventilation (-0.0 L/min; 95% CI, -0.2 to 0.2 L/mi

12 improvement of 21.6 mm Hg (CO2), 168 mL/sec (minute ventilation), 0.25 mL/kg (airway opening tidal vo

13 y pressure, 24.8+/-2.4 to 13.7+/-0.7 cm H2O; minute ventilation, 12.7+/-1.4 to 6.2+/-0.8 L/min; respi

14 Hypoglycaemia significantly augmented minute ventilation (123 +/- 4 to 143 +/- 7 ml min(-1) )

15 ) had higher FIO2 (0.65 vs. 0.44, p = .006), minute ventilation (14.6 vs. 9.9 L/min, p = .005), posit

16 adrenaline (1 mug kg(-1) min(-1) ) increased minute ventilation (145 +/- 4 to 173 +/- 5 ml min(-1) )

17 Minute ventilation (29 +/- 8 versus 21 +/- 6 L/min, p <

18 , patients with OSA had greater increases in minute ventilation (5.8+/-0.8 versus 3.2+/-0.7 L/min; P=

19 s 20.5+/-7 mL x min[-1] x kg[-1] [placebo]), minute ventilation (57.5+/-17 [enalapril] versus 55.4+/-

20 .3 kPa]; p = .005) without affecting expired minute ventilation (6.2 +/- 0.4 to 6.5 +/- 0.4 L/min; p

21 , patients with CHF had greater increases in minute ventilation (6.7+/-1.4 versus 2.7+/-0.9 L/min, P=

22 /-16 yr vs. 54+/-17 yr, p<0.01) with a lower minute ventilation (8.8+/-2.2 L/min vs. 10.1+/-2.9 L/min

23 Both healthy and injured sheep reduced minute ventilation according to the amount of extracorpo

24 Breathing abnormalities include decreased minute ventilation and a specific loss of sighs, which w

25 e magnitude of adenosine evoked responses in minute ventilation and blood pressure was analogous to t

26 d artery causes a dose-dependent increase in minute ventilation and blood pressure with a concomitant

27 epinephrine was significantly lower, whereas minute ventilation and exhaled CO2 were significantly in

28 While monitoring minute ventilation and heart rate, exercise challenge wa

29 reathing during CPAP with the helmet; and c) minute ventilation and Pco2 should be monitored during C

30 riables that affect CO2 elimination, such as minute ventilation and peak airway pressure (peak Paw) a

31 venous shunt allows significant reduction in minute ventilation and peak inspiratory pressure without

32 Once a panic attack is triggered, minute ventilation and respiratory rate increase regardl

33 dioxide challenge, probands exhibited larger minute ventilation and respiratory rate responses relati

34 7 ppm) concentration was found at the lowest minute ventilation and the largest inspiratory circuit v

35 VE (minute ventilation) and the ratio VE/VCO2 (ventilation r

36 lood flow (FBF), heart rate, blood pressure, minute ventilation, and end-tidal CO(2) were determined.

37 nd it increased fractional inspiratory time, minute ventilation, and mean inspiratory flow (all p < o

38 Still, overall mean respiratory rate, minute ventilation, and sleep architecture were equivale

39 ) and placebo infusion on oxygen saturation, minute ventilation, and sympathetic nerve activity durin

40 , peak inspiratory flow rate demand, exhaled minute ventilation, and the duration of respiratory musc

41 ship between lung volume and carbon dioxide, minute ventilation, and tidal volume (both at airway ope

42 electroencephalography, electro-oculography, minute ventilation, arterial blood gases, and serum theo

43 pecific to acute lung injury, and identified minute ventilation as a potential novel predictor of dea

44 p were induced to hyperventilate to the same minute ventilation as during exercise, using modest CO2

45 Low end-tidal CO2 and high variance in minute ventilation at baseline predicted panic attacks d

46 tly decreased respiratory rate and decreased minute ventilation at peak exercise.

47 xide was considered to be the point at which minute ventilation began to rise in a linear fashion as

48 eous measurements of pulmonary gas exchange, minute ventilation, blood lactate, and quadriceps muscle

49 N and C lambs had similar minute ventilation but a markedly different breathing pa

50 pared with baseline, R-ED and ECCO2R reduced minute ventilation by 50% and 27%, respectively.

51 ve to saline, SCH-treated hamsters decreased minute ventilation by decreasing tidal volume and oxygen

52 0 breaths/min, compared with CMV at the same minute ventilation, can improve CO2 exchange.

53 n 62% (IQR, 45-77%) of predicted, and median minute ventilation/carbon dioxide production slope 34.9

54 eak oxygen consumption predicted, and higher minute ventilation/carbon dioxide production slope.

55 ues of predicted peak oxygen consumption and minute-ventilation/carbon dioxide production slope, whic

56 Minute ventilation/CO(2) production (VE/Vco(2)) slope is

57 clonidine, 2.6 +/- 0.2 mEq/L), and decreased minute ventilation (control, 39.7 +/- 2.1 versus clonidi

58 matched control subjects, dopamine decreased minute ventilation despite decreased oxygen saturation a

59 Asthma mice showed significant impairment in minute ventilation despite increased peak expiratory flo

60 Minute ventilation determined CO2 clearance during perfl

61 Compensatory increases in minute ventilation during exercise maintained alveolar v

62 Dopamine did not decrease minute ventilation during normoxia in normal subjects.

63 gated the effects of dopamine and placebo on minute ventilation during normoxic breathing in 8 patien

64 ulted in consistently lower tidal volume and minute ventilation during test circuit activities.

65 ng 8% CO2 elicited a moderate hyperpnea, and minute ventilation during the final minute of CO2 breath

66 Baseline measures of minute ventilation during the placebo and antioxidant tr

67 ia (calculated as the difference between the minute ventilation during the second full minute of hypo

68 Peak oxygen uptake increased and heart rate, minute ventilation, dyspnea, and leg fatigue decreased a

69 of HFNC on gas exchange, inspiratory effort, minute ventilation, end-expiratory lung volume, dynamic

70 ses, as well as with levels of tidal volume, minute ventilation, end-tidal CO(2), and irregularity in

71 8 to 14.2 +/- 3.5 (p < 0.01) breaths/min and minute ventilation from 10.4 +/- 1.6 to 4.9 +/- 1.7 L/mi

72 Lowering tidal volume to 4 mL/kg reduced minute ventilation from 7.8 +/- 1.5 to 5.2 +/- 1.1 L/min

73 es) on MSNA, heart rate, blood pressure, and minute ventilation in 14 untreated patients with OSA and

74 HeO2 resulted in the greatest maximum minute ventilation in both bike and KE (p < 0.05) but ha

75 ed expiratory flow, breathing frequency, and minute ventilation in both groups (p < 0.05).

76 exercise is associated with abnormally high minute ventilation in patients with CHF and with a limit

77 reathing frequency, tidal volume, and, thus, minute ventilation in response to a respiratory challeng

78 emicircular canals by yaw rotation increased minute ventilation in young but not older subjects.

79 tion in patients with CHF and with a limited minute ventilation increase in patients with COPD, funct

80 his apnea suppression normalized inspiratory minute ventilation increased during all wake/sleep state

81 m 7.04+/-0.07 to 7.31+/-0.15 (p = .0012) and minute ventilation increased from 0.66+/-0.40 to 4.00+/-

82 Normalized inspiratory minute ventilation increased significantly during wakefu

83 Minute ventilation increased significantly for 30 minute

84 he respiratory stimulating effect of 7% CO2; minute ventilation increased to 250 +/- 17 ml/min before

85 Minute ventilation influences clearance of CO2.

86 or induced acute cerebral hypoxia-ischemia, minute ventilation initially increased, and then hypopne

87 is effect is relatively modest when baseline minute ventilation is < or = 10 L/min, because of the lo

88 ethysmography; polymorphonuclear leukocytes; minute ventilation; knockout mice; methacholine

89 breathing, probands had significantly larger minute ventilation, larger tidal volumes, and more varia

90 The breathing reserve index (BRI = minute ventilation/maximal voluntary ventilation) at the

91 scutaneous carbon dioxide, tidal volume, and minute ventilation may assist in refining strategies to

92 in Heart Failure) trial investigated whether minute ventilation (MV) adaptive servo-ventilation (ASV)

93 f four levels of spontaneous breath in total minute ventilation (n = 9 per group, 6 hr each): 1) biph

94 respiratory rate often sufficient to sustain minute ventilation near baseline levels, without arousal

95 At a constant minute ventilation, nitric oxide inhalation caused dose-

96 (FIO2, positive end-expiratory pressure, and minute ventilation) occurred in patients fed EPA+GLA com

97 taneous breathing, these data were observed: minute ventilation of < 10 L/min; resting respiratory ra

98 with and without the mixing chambers, with a minute ventilation of 14 L/min and a nitric oxide concen

99 piratory fluctuations and was highest with a minute ventilation of 21 L/min and higher during pressur

100 In each mode, minute ventilation of 7, 14, and 21 L/min and installati

101 , p < .05) despite a lack of any increase in minute ventilation or respiratory rate.

102 s no difference in oxygenation, ventilation, minute ventilation, or pH after tracheostomy.

103 However, ventilatory equivalents (minute ventilation/oxygen consumption) revealed signific

104 Hypoxia increased heart rate (P < 0.05) and minute ventilation (P < 0.05) at rest and exercise under

105 Significant differences were found in minute ventilation (p = 0.006), temperature-corrected Pa

106 logy score, age, comorbidities, arterial pH, minute ventilation, PaCO2, PaO2/FiO2 ratio, intensive ca

107 Different methods for estimating minute ventilation performed well in relative terms with

108 t of a spontaneous breath, fraction of total minute ventilation provided by the ventilator, and mean

109 genation index, increasing fraction of total minute ventilation provided by the ventilator, increasin

110 essure, oxygenation index, fraction of total minute ventilation provided by the ventilator, peak vent

111 oxygenation index, and the fraction of total minute ventilation provided by the ventilator.

112 oxygenation index, and the fraction of total minute ventilation provided by the ventilator.

113 /- 4 vs. He 18 +/- 5 ml/kg per min) and peak minute ventilation (RA 53 +/- 12 vs. He 53 +/- 15 liters

114 RA 724 +/- 163 vs. He 762 +/- 123 s) or peak minute ventilation (RA 97 +/- 27 vs. He 97 +/- 28 liters

115 al practice, that is, more than 30% of total minute ventilation, reduced lung injury with improved re

116 effectiveness of TGI, provided that inspired minute ventilation remains unchanged and end-expiration

117 espiratory parameters (ventilatory settings, minute ventilation, respiratory rate, airway pressures)

118 Men and women had near identical minute ventilation responses to total load (applied extr

119 ); however, because the males had 45% higher minute ventilations than the females, the deposition rat

120 Minute ventilation, tidal volume, and breathing frequenc

121 EE, substrate utilization, minute ventilation, tidal volume, and respiratory rate w

122 /min (96% of total CO2 production), allowing minute ventilation to be reduced from 10.3 +/- 1.4 L/min

123 Peak Vo(2), E/CO2 slope (ratio of minute ventilation to carbon dioxide production), and he

124 es hypoventilation (decrease in the ratio of minute ventilation to oxygen consumption, V(E)/V(O2)) an

125 erence can be corrected easily by increasing minute ventilation until expired tidal volume equals des

126 Minute ventilation ( V E) increased following all trials

127 in infusion (30 microg/d) markedly increased minute ventilation (V E) across all sleep/wake states, b

128 correlation between the increase in baseline minute ventilation (V E) and hyperleptinemia (r = 0.77,

129 We assessed minute ventilation (V E) at rest and during hypercapnic

130 Ro 32-0432 decreased minute ventilation (V E) by 51.0 +/- 5.5% (mean +/- SEM)

131 During O(3) exposure (1 pm, 3 h), minute ventilation (V E) decreased by 64 +/- 4% in wild-

132 DA receptors during development, we measured minute ventilation (V E) in 5-d, 10-d, and 15-d-old inta

133 We previously observed an increase in minute ventilation (V E) with resistive unloading (He-O2

134 O(2)), carbon dioxide production (V CO(2)), minute ventilation (V E), and tidal volume (VT) between

135 the selective MOR agonist DAMGO, analgesia, minute ventilation (V E), heart rate (HR) and mean arter

136 Minute ventilation (V E), lung volume, and expiratory ai

137 eathing pattern at maximal exercise: maximal minute ventilation (V Emax) (r = -0.47; p = 0.009), and

138 aximal oxygen consumption (V O2max), maximal minute ventilation (V Emax), and maximum voluntary venti

139 upward shift in the CO2-response curves for minute ventilation (V I) and frequency (f ), and a signi

140 c hypoxia increased the gross variability of minute ventilation (V I), tidal volume (VT), inspiratory

141 ational activity of expiratory time (TE) and minute ventilation (V I), whereas a load of 6 cm H2O/L/s

142 Minute ventilation (V(E)) in 2, 4, and 6% CO(2) was meas

143 Inspired minute ventilation (V(I)), R(UA) and end-tidal CO(2) pre

144 ecline, whereas both tidal volume (V(T)) and minute ventilation (.V(E) ) significantly increased in t

145 Ten male subjects were asked to breathe at minute ventilation (V1) equal or slightly greater than 6

146 Here we define a pathway in which increased minute ventilation (&Vdot;E ) is signalled by deoxyhaemo

147 tion (EOV) refers to regular oscillations in minute ventilation (VE) during exercise.

148 ed by correlating CO2 production (V(CO2)) to minute ventilation (VE) in each test.

149 ller, the regression line for the P(a,CO(2))-minute ventilation (VE) relation shifted to higher VE an

150 Post-C5 SCI rats demonstrated deficits in minute ventilation (Ve) responses to a 7% CO2 challenge

151 Minute ventilation (VE) was measured using whole-body pl

152 f humans as a function of concentration (C), minute ventilation (VE), duration of exposure (T), and a

153 achieved by generating significantly larger minute ventilation (VE), from 24 +/- 11 to 29 +/- 10 L/m

154 We determined minute ventilation (VE), oxygen consumption (VO2), carbo

155 ilatory efficiency, commonly assessed by the minute ventilation (VE)-carbon dioxide production (VCO2)

156 is predominantly reported as an increase in minute ventilation (VE).

157 abnormal, characterized by elevation of the minute ventilation (VE)/CO(2) elimination slope (VE/VCO(

158 , range 6 to 44 watts, p < 0.05) and maximal minute ventilation (VEmax) increased by a median of 22%

159 d signaling is involved in the regulation of minute ventilation, ventilation-perfusion matching, pulm

160 ting in a NREM sleep-associated decrement in minute ventilation (VI = 11.10 +/- 0.67, 9.32 +/- 0.91,

161 air, CO2 increased the gross variability of minute ventilation (VI) and tidal volume (VT), and decre

162 CO2 response slopes were increased 303% for minute ventilation (VI)(P </= 0.01) and 251% for mean in

163 ptors by acute hypoxia causes an increase in minute ventilation (VI), heart rate (HR) and arterial bl

164 In the morbidly obese, at high minute ventilations, VO(2RESP) is greater than in normal

165 CH rats breathing 12% O2 had greater minute ventilation (VP) than N rats breathing air, but t

166 vel bicycle and treadmill exercise such that minute ventilation was <25 l/min.

167 During hypoxia, minute ventilation was 12.9+/-1.3 L/min on dopamine and

168 Minute ventilation was determined during each minute of

169 In all 3 periods, minute ventilation was higher in the CF and CFDM groups

170 ere were no differences in hemodynamics, but minute ventilation was lower in the AVCO2R group and Pac

171 Minute ventilation was lowered to less than half of its

172 Minute ventilation was maintained constant at each tidal

173 Minute ventilation was recorded during infusion of insul

174 During HFNC, minute ventilation was reduced (P < 0.001) at constant a

175 To maintain normocapnia, minute ventilation was reduced from 3.8 +/- 0.1 L/min to

176 Minute ventilation was reduced from 5.6 L/min at baselin

177 Minute ventilation was reduced to induce hypercapnia wit

178 Minute ventilation was reduced, and normocarbia (Paco2 3

179 Minute ventilation was smaller with the impedance system

180 Minute ventilation was then altered by adjusting tidal v

181 r study, ITPV, compared with CMV at the same minute ventilation, was associated with a significantly

182 Inspiratory time (0.75 sec), FIO2 (0.3), and minute ventilation were held constant.

183 Respiratory rate, tidal volume, and minute ventilation were studied to determine their effec

184 gh arousal threshold, may be able to sustain minute ventilation when challenged with negative airway

185 Dex-Asthma mice compensated to maintain high minute ventilation, whereas Asthma mice showed significa

186 enous CO2 removal enabled a 50% reduction in minute ventilation while maintaining normocarbia and may

187 real venovenous CO2 removal device to reduce minute ventilation while maintaining normocarbia.