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 evoked an increase in ventilation that resulted in

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

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

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

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

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

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

11 in men than women during static handgrip and LBNP.

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

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

14 single units increased during both LBPP and LBNP.

15 tractions (engages only muscle reflexes) and LBNP.

16 30% maximum voluntary contraction (MVC); (b) LBNP at -10 and -30 mmHg (each level for 5 min); and (c)

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

18 le mechanoreflex) and a circuit activated by LBNP.

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

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

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

22 During LBNP, MSNA responses were attenuated after melatonin at

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

24 aroreceptor sensitivity were assessed during LBNP using plethysmography.

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

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

27 t frequency, and total MSNA increased during LBNP.

28 responses were unchanged by melatonin during LBNP.

29 5 min); and (c) 15 s HG (at 30% MVC) during LBNP at both levels.

30 e similar levels of arterial pressure during LBNP.

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

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

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

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

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

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

37 striction or paradoxical vasodilation during LBNP.

38 decreases in RV end-diastolic volume during LBNP.

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

40 no statistical change throughout the entire LBNP protocol.

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

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

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

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

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

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

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

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

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

50 activity (MSNA) relationships during intense LBNP.

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

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

53 hanges after the abrupt cessation of maximal LBNP.

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

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

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

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

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

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

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

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

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

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

64 rom positive to negative with application of LBNP.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 patients whilst the remaining 70 % required LBNP.

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

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

111 vascular resistance (FVR) during submaximal LBNP.

112 10 min combined HUT and lower body suction (LBNP) at -20 mmHg followed by LBNP at -40 mmHg.

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

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

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

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

117 123 +/- 8, 121 +/- 10, 131 +/- 7 ml prior to LBNP, during normothermia, skin-surface cooling, and who

118 mal administration of isoproterenol prior to LBNP.

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

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

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

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

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

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

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

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

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

128 tation during central volume unloading using LBNP.

129 s not prevent the presyncope associated with LBNP.

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

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

132 FVR increased with LBNP after placebo.

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

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