ライフサイエンスコーパス: LBNP

1 LBNP and LBPP had no heart rate, stroke volume, or blood

2 LBNP decreased pulse pressure, but did not change mean a

3 LBNP did not affect cerebrovascular CO2 response slopes

4 LBNP during sleep may be an effective countermeasure for

5 LBNP evoked an increase in ventilation that resulted in

6 LBNP from 0 to 50 mmHg at increments of 10 mmHg lowered

7 LBNP of 30 mmHg induced greater decreases in SV during h

8 LBNP provoked a larger decrease in SV relative to the de

9 LBNP reduced CVC at the BTX-A-treated sites (Delta4.2 +/

10 Across LBNP stages, IHH further enhanced ejection fraction (Del

11 (p < .001) and pulse (p < .001) 3 mins after LBNP.

12 An LBNP of 20 mmHg may be the optimal level to lower ICP wi

13 The CPT and LBNP further increased MSNA burst frequency and burst in

14 ressure, and heart rate responses to CSM and LBNP were measured at baseline and at 6 weeks.

15 in men than women during static handgrip and LBNP.

16 m the responses noted during combined HG and LBNP (17 +/- 6% at -10 mmHg and 25 +/- 8% at -30 mmHg).

17 However, the effect of simultaneous HG and LBNP on the renal circulation in humans is not known.

18 single units increased during both LBPP and LBNP.

19 tractions (engages only muscle reflexes) and LBNP.

20 We applied LBNP while recording ICP and blood pressure while supine

21 30% maximum voluntary contraction (MVC); (b) LBNP at -10 and -30 mmHg (each level for 5 min); and (c)

22 Before LBNP, SV was not affected by heating (122 +/- 30 ml; mea

23 le mechanoreflex) and a circuit activated by LBNP.

24 body suction (LBNP) at -20 mmHg followed by LBNP at -40 mmHg.

25 g kg(-1)) or unaltered (placebo) followed by LBNP to pre-syncope.

26 he lower body in a negative pressure device (LBNP) that pulls fluid away from cranial compartments, w

27 During LBNP while heat stressed, the reductions in blood volume

28 During LBNP, MSNA responses were attenuated after melatonin at

29 During LBNP, the ratio of single units with anticipated and par

30 ial: p = 0.27, interaction: p = 0.39) during LBNP stages were no different between trials.

31 c resonance angiography (MRA) at 1.5T during LBNP at 0, -20 and -40 mmHg, and were assigned to VAH (n

32 aroreceptor sensitivity were assessed during LBNP using plethysmography.

33 ICA flow decreased during LBNP (P < 0.0001) and was not different between groups.

34 Total CBF decreased during LBNP in hypertensives without VAH (P = 0.0192 at -20 mmH

35 Changes in FVR during LBNP (-20 and -30 mm Hg) were markedly attenuated in the

36 alcohol intake, FVR did not increase during LBNP despite the potentiated decrease in blood pressure.

37 peripheral resistance (TPR) increased during LBNP in both groups, but the rise was greater in the gro

38 t frequency, and total MSNA increased during LBNP.

39 responses were unchanged by melatonin during LBNP.

40 5 min); and (c) 15 s HG (at 30% MVC) during LBNP at both levels.

41 e similar levels of arterial pressure during LBNP.

42 the reduction in the SV to PCWP ratio during LBNP was comparable to that observed during normothermia

43 BA flow was reduced during LBNP in the group without VAH (P = 0.0267 at -20 mmHg an

44 had normal vasoconstrictor responses during LBNP (FVR increased by 7.7 +/- 4.9 U).

45 versed paradoxical vascular responses during LBNP in seven (78%) patients from group A.

46 FVR responses during LBNP were reduced during alcohol compared with placebo c

47 pressure did not change significantly during LBNP at -5, -10, and -20 mm Hg.

48 Paradoxical vasodilatation during LBNP occurs in 40% of patients with ABPR during exercise

49 striction or paradoxical vasodilation during LBNP.

50 decreases in RV end-diastolic volume during LBNP.

51 rdiovascular collapse in each subject (i.e., LBNP maximum).

52 no statistical change throughout the entire LBNP protocol.

53 s normalised maximal tolerance by expressing LBNP levels as 80, 60, 40, 20 and 0% (baseline) of maxim

54 Furthermore, LBNP holds clinical potential as a safe, non-invasive me

55 were greater in men vs. women during graded LBNP (P < 0.04).

56 ed during all levels of LBNP in both groups (LBNP main effect P < 0.0001), whereas MAP was reduced in

57 etween the time to presyncope from -50 mm Hg LBNP (equivalent to 60 degrees HUT alone) and the change

58 tolic volumes were assessed during -30 mm Hg LBNP in all heart failure patients.

59 d in 5 of these 12 patients during -30 mm Hg LBNP, a response seen in none of the remaining patients

60 lower-body negative pressure (to -50 mm Hg; LBNP) was used to examine the integrated baroreflex resp

61 In the hypertensives, LBNP evoked decreases in oxygenation and FBF that were s

62 ect of L-NAME was counteracted by increasing LBNP to -40 mmHg (+19 +/- 2 bursts min(-1)).

63 Application of incremental LBNP demonstrated a non-linear dose-response curve, sugg

64 f venous return, probably induced by intense LBNP, disrupt MSNA firing characteristics that manifest

65 activity (MSNA) relationships during intense LBNP.

66 therefore tested the hypotheses that intense LBNP disrupts MSNA firing characteristics and leads to a

67 d in the group with VAH (P > 0.05 all levels LBNP).

68 Likewise, LBNP at -40 mmHg decreased muscle oxygenation both in re

69 hanges after the abrupt cessation of maximal LBNP.

70 as significantly decreased at 50% of maximum LBNP while SmO2 (UMMS) decreased at 75% of maximum LBNP.

71 hile SmO2 (UMMS) decreased at 75% of maximum LBNP.

72 The CCR5-mediated LBNP cell uptake and retention reduce HIV-1 replication

73 Subjects were exposed to 5 min LBNP stages until the onset of presyncope.

74 near dose-response curve, suggesting 20 mmHg LBNP as the optimal level for reducing pressure in the b

75 Seven subjects underwent 30 mmHg LBNP while normothermic, during passive heat stress (inc

76 Before L-NAME, LBNP at -20 mmHg decreased muscle oxygenation by 20 +/-

77 After L-NAME, LBNP at -20 mmHg decreased muscle oxygenation similarly

78 ulation in which a lipid-based nanoparticle (LBNP) carrying rilpivirine (RPV) is decorated with the C

79 Nightly LBNP caused a sustained reduction in supine central veno

80 Nightly LBNP reinstated a footward fluid shift and mitigated the

81 Eight hours of nightly LBNP (-20 mm Hg) vs no LBNP.

82 t with and 3 days without 8 hours of nightly LBNP in a randomized, crossover design.

83 ight hours of nightly LBNP (-20 mm Hg) vs no LBNP.

84 hyper- and hypocapnia during the LBNP and no-LBNP conditions.

85 In the normotensives, LBNP caused decreases in oxygenation and FBF (-16 +/- 2%

86 While normothermic,LBNP reduced blood volume in all regions (torso: 22 +/-

87 volume was significantly decreased at 25% of LBNP maximum, whereas blood pressure was a late indicato

88 d ICP to 26 +/- 4 mmHg, while application of LBNP lowered ICP (to 21 +/- 4, 20 +/- 4, 18 +/- 4, 17 +/

89 rom positive to negative with application of LBNP.

90 ll values were normalized to the duration of LBNP exposure required for cardiovascular collapse in ea

91 05 for all, post hoc), but not at the end of LBNP.

92 (P<.01 for both comparisons at each level of LBNP).

93 s fused in 10 subjects during high levels of LBNP (burst fusing may reflect modulation of central mec

94 lower in LT relative to HT at all levels of LBNP (P < 0.05).

95 pressure fell significantly at all levels of LBNP during the alcohol session.

96 The CO decreased during all levels of LBNP in both groups (LBNP main effect P < 0.0001), where

97 egrated baroreflex response to low levels of LBNP was characterized by shorter R-R intervals and more

98 patients with VAH (P > 0.05 at all levels of LBNP).

99 At each stage of LBNP and albumin infusion was measured using an acetylen

100 tion or vagotonia associated with a positive LBNP response and had no significant effect on barorefle

101 Seven out of 9 subjects who had a positive LBNP response at baseline had a repeat positive LBNP res

102 P response at baseline had a repeat positive LBNP response, and the subject with a positive CSM at ba

103 nificant difference between initial and post-LBNP cardiac index (p > .05).

104 of progressive lower body negative pressure (LBNP) (-15, -30 and -45 mmHg) before and after IHH.

105 ributions with lower body negative pressure (LBNP) are similar to those that occur during haemorrhage

106 uring 5 min of lower body negative pressure (LBNP) at -10 and -40 mmHg (n = 11).

107 n, produced by lower body negative pressure (LBNP) at -40 mmHg, on cerebrovascular responsiveness to

108 SNA) evoked by lower body negative pressure (LBNP) at rest and during moderate-intensity rhythmic han

109 oreflexes with lower body negative pressure (LBNP) can engage the sympathetic nervous system (SNS).

110 oring with the lower body negative pressure (LBNP) device.

111 as reduced via lower-body negative pressure (LBNP) during normothermia, whole-body heating (increase

112 ivation during lower body negative pressure (LBNP) evoked decreases in muscle oxygenation in resting

113 e increases in lower-body negative pressure (LBNP) in 14 healthy young volunteers.

114 sponses during lower body negative pressure (LBNP) in 21 non-obstructive hypertrophic cardiomyopathy

115 and -30 mm Hg lower-body negative pressure (LBNP) in 24 patients with chronic heart failure and 16 c

116 A validated lower body negative pressure (LBNP) model was used to induce progression towards hypov

117 a progressive lower body negative pressure (LBNP) protocol designed to cause presyncope in all subje

118 ssage (CSM) or lower body negative pressure (LBNP) received Paxil (20 mg/d) or placebo for 6 weeks.

119 Lower body negative pressure (LBNP) simulates the effects of gravity by displacing flu

120 nitial maximal lower body negative pressure (LBNP) test to place them into a low (LT, n = 7, 22 +/- 1

121 Progressive lower body negative pressure (LBNP) to onset of cardiovascular collapse.

122 by progressive lower-body negative pressure (LBNP) to presyncope.

123 nt progressive lower-body negative pressure (LBNP) until pre-syncope; end-tidal carbon dioxide (P ET

124 d using graded lower-body negative pressure (LBNP) until the onset of symptoms associated with ensuin

125 test (CPT) and lower body negative pressure (LBNP) were superimposed upon heating.

126 (PCWP), during lower-body negative pressure (LBNP) while subjects are normothermic, during skin-surfa

127 mplished using lower body negative pressure (LBNP), while increases in were accomplished using infusi

128 tion evoked by lower body negative pressure (LBNP).

129 sure are lowered via body negative pressure (LBNP).

130 ge imposed via lower-body negative pressure (LBNP).

131 rves evoked by lower body negative pressure (LBNP).

132 nonhypotensive lower body negative pressure (LBNP; -10 mm Hg) and nonhypertensive positive pressure (

133 application of lower body negative pressure (LBNP; -30 mmHg).

134 intervention, lower body negative pressure (LBNP; 3 min at -15, -30 and -45 mmHg) was applied to eli

135 ed progressive lower-body negative pressure (LBNP; a validated model for simulating haemorrhage) test

136 during graded lower body negative pressure (LBNP; activates baroreflex-mediated sympathetic system)

137 ts experienced lower-body negative-pressure (LBNP) of 0, 15 and 30 mmHg during normothermia, skin-sur

138 usly mediated (lower body negative pressure [LBNP]) and exogenously mediated (brachial artery infusio

139 olemic stress (lower body negative pressure [LBNP]) in healthy human males.

140 port three primary findings: (1) progressive LBNP (and presumed progressive arterial baroreceptor unl

141 roke volume were obtained during progressive LBNP with simultaneous assessments of StO2, PmO2, and mu

142 patients whilst the remaining 70 % required LBNP.

143 ilarly, when flow was matched between sites, LBNP reduced CVC at both the BTX-A-treated (Delta15.3 +/

144 sitivity, 87.5% specificity) at the smallest LBNP change (0-15 mmHg).

145 During submaximal LBNP, FVR increased in HT (ANOVA P < 0.05) but not in LT

146 vascular resistance (FVR) during submaximal LBNP.

147 10 min combined HUT and lower body suction (LBNP) at -20 mmHg followed by LBNP at -40 mmHg.

148 er (BBB) disruption allows the CCR5-targeted LBNP to penetrate the BBB and reach brain myeloid cells.

149 cing fluid caudally and we hypothesized that LBNP would lower ICP without compromising cerebral perfu

150 The LBNP level eliciting presyncope was denoted as 100% tole

151 arately for hyper- and hypocapnia during the LBNP and no-LBNP conditions.

152 ate (electrocardiogram) responses during the LBNP test using a mixed effects model (time [LBNP stage]

153 Tolerance to the LBNP test was not different between trials (Ketamine: 63

154 The best vital sign metric (MAP) at this LBNP change yielded an AUC of 0.6 (CI 0.38-0.79, 100% se

155 LBNP test using a mixed effects model (time [LBNP stage] x drug).

156 egion were markedly greater when compared to LBNP while normothermic (torso: 73 +/- 2%; heart: 72 +/-

157 day, dextran 40 was rapidly infused prior to LBNP sufficient to return central venous pressure to pre

158 123 +/- 8, 121 +/- 10, 131 +/- 7 ml prior to LBNP, during normothermia, skin-surface cooling, and who

159 mal administration of isoproterenol prior to LBNP.

160 The increment in muscle SNA in response to LBNP at -20 mmHg also was attenuated after L-NAME (befor

161 when infused alone, but the FABF response to LBNP in the infused arm was attenuated during the perind

162 cts continued to have a positive response to LBNP with presyncope.

163 mL x dL forearm(-1) x min(-1)) responses to LBNP (-20 cm H2O) and increasing increments of norepinep

164 hol potentiated the hypotensive responses to LBNP, particularly at -40 mm Hg, when the decrease in sy

165 t of the reduction in these blood volumes to LBNP relative to heat stress alone (torso: 73 +/- 1%; he

166 When these subjects became nitrate tolerant, LBNP-induced decreases in muscle oxygenation were unaffe

167 Maximal tolerated LBNP produced reductions in cardiac, stroke, and contrac

168 Subjects underwent two LBNP exposures terminated by the onset of vasodepression

169 tation during central volume unloading using LBNP.

170 s not prevent the presyncope associated with LBNP.

171 The decrease in CVP with LBNP was correlated with the reduction in PCWP during no

172 mated central venous pressure decreased with LBNP (P<0.05), increased with LBPP (P<0.05), and was con

173 FVR increased with LBNP after placebo.

174 In contrast, in eight postmenopausal women, LBNP decreased muscle oxygenation by 15 +/- 3% in restin

175 In eight premenopausal women, LBNP decreased muscle oxygenation by 20 +/- 1% in restin