Arterial diameter during central volume depletion in humans

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Arterial diameter during central volume depletion in humans. / Iversen, Helle Klingenberg; Madsen, P; Matzen, S; Secher, N H.

In: European Journal of Applied Physiology and Occupational Physiology, Vol. 72, No. 1-2, 1995, p. 165-9.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Iversen, HK, Madsen, P, Matzen, S & Secher, NH 1995, 'Arterial diameter during central volume depletion in humans', European Journal of Applied Physiology and Occupational Physiology, vol. 72, no. 1-2, pp. 165-9.

APA

Iversen, H. K., Madsen, P., Matzen, S., & Secher, N. H. (1995). Arterial diameter during central volume depletion in humans. European Journal of Applied Physiology and Occupational Physiology, 72(1-2), 165-9.

Vancouver

Iversen HK, Madsen P, Matzen S, Secher NH. Arterial diameter during central volume depletion in humans. European Journal of Applied Physiology and Occupational Physiology. 1995;72(1-2):165-9.

Author

Iversen, Helle Klingenberg ; Madsen, P ; Matzen, S ; Secher, N H. / Arterial diameter during central volume depletion in humans. In: European Journal of Applied Physiology and Occupational Physiology. 1995 ; Vol. 72, No. 1-2. pp. 165-9.

Bibtex

@article{d3824e15a3c94cbeb176fa90aba76dd7,
title = "Arterial diameter during central volume depletion in humans",
abstract = "The luminal diameter of the radial artery was followed by high frequency ultrasound during 50 degrees head-up tilt-induced central volume depletion in ten healthy subjects of whom six were tilted twice and pretreated with the serotonin receptor antagonist methysergide or placebo following a double-blind randomized design. Eight subjects without active treatment experienced presyncopal symptoms after 16-45 (mean 32 min). Central volume depletion was indicated by an increase in mean thoracic electrical impedance [from 31.5 (SEM 1.6) to 33.4 (SEM 1.7) omega; P < 0.05]. Cardiac output decreased [from 4.1 (SEM 0.3) to 2.2 (SEM 0.3) 1.min-1] and heart rate [HR, from 64 (SEM 3) to 100 (SEM 7) beats.min-1], mean arterial pressure (MAP, from 77 (SEM 4) to 89 (SEM 2) mmHg [10.3 (SEM 0.53 to 11.9 (SEM 0.27) kPa]) and total peripheral resistance (TPR, from 19 (SEM 2) to 34 (SEM 4) mmHg.min.1-1 [2.5 (SEM 0.27) to 4.5 (SEM 0.53) kPa.min.1-1]) increased; but with the appearance of presyncopal symptoms, HR, MAP and TPR were reduced to 65 (SEM 8) beats.min-1, 46 (SEM 4) mmHg [6.1 (SEM 0.53) kPa] and 18 (SEM 3) mmHg.min.1-1 [2.4 (SEM 0.4) kPa.min-1.1-1], respectively (P < 0.05). Vascular resistance was reflected in the arterial diameter which decreased from 2.42 (SEM 0.17) to 2.27 (SEM 0.14) mm during head-up tilt and increased to 2.71 (SEM 0.14) mm with the appearance of presyncopal symptoms (P < 0.05). Methysergide reduced the resting radial (15 +/- 2%) and temporal artery diameters (10 +/- 3%) (P < 0.05); however, it affected neither tilt-tolerance nor the central cardiovascular response to tilt. The results suggested a serotonergic influence on arterial tone at rest, and demonstrated that vessels as large as the radial artery participated in vascular control during central volume depletion independent of such a serotonergic influence.",
keywords = "Adult, Blood Pressure, Blood Volume, Cardiac Output, Double-Blind Method, Electric Impedance, Female, Heart Rate, Humans, Male, Methysergide, Placebos, Posture, Radial Artery, Serotonin Antagonists, Vascular Resistance",
author = "Iversen, {Helle Klingenberg} and P Madsen and S Matzen and Secher, {N H}",
year = "1995",
language = "English",
volume = "72",
pages = "165--9",
journal = "European Journal of Applied Physiology and Occupational Physiology",
issn = "0301-5548",
publisher = "Springer Verlag",
number = "1-2",

}

RIS

TY - JOUR

T1 - Arterial diameter during central volume depletion in humans

AU - Iversen, Helle Klingenberg

AU - Madsen, P

AU - Matzen, S

AU - Secher, N H

PY - 1995

Y1 - 1995

N2 - The luminal diameter of the radial artery was followed by high frequency ultrasound during 50 degrees head-up tilt-induced central volume depletion in ten healthy subjects of whom six were tilted twice and pretreated with the serotonin receptor antagonist methysergide or placebo following a double-blind randomized design. Eight subjects without active treatment experienced presyncopal symptoms after 16-45 (mean 32 min). Central volume depletion was indicated by an increase in mean thoracic electrical impedance [from 31.5 (SEM 1.6) to 33.4 (SEM 1.7) omega; P < 0.05]. Cardiac output decreased [from 4.1 (SEM 0.3) to 2.2 (SEM 0.3) 1.min-1] and heart rate [HR, from 64 (SEM 3) to 100 (SEM 7) beats.min-1], mean arterial pressure (MAP, from 77 (SEM 4) to 89 (SEM 2) mmHg [10.3 (SEM 0.53 to 11.9 (SEM 0.27) kPa]) and total peripheral resistance (TPR, from 19 (SEM 2) to 34 (SEM 4) mmHg.min.1-1 [2.5 (SEM 0.27) to 4.5 (SEM 0.53) kPa.min.1-1]) increased; but with the appearance of presyncopal symptoms, HR, MAP and TPR were reduced to 65 (SEM 8) beats.min-1, 46 (SEM 4) mmHg [6.1 (SEM 0.53) kPa] and 18 (SEM 3) mmHg.min.1-1 [2.4 (SEM 0.4) kPa.min-1.1-1], respectively (P < 0.05). Vascular resistance was reflected in the arterial diameter which decreased from 2.42 (SEM 0.17) to 2.27 (SEM 0.14) mm during head-up tilt and increased to 2.71 (SEM 0.14) mm with the appearance of presyncopal symptoms (P < 0.05). Methysergide reduced the resting radial (15 +/- 2%) and temporal artery diameters (10 +/- 3%) (P < 0.05); however, it affected neither tilt-tolerance nor the central cardiovascular response to tilt. The results suggested a serotonergic influence on arterial tone at rest, and demonstrated that vessels as large as the radial artery participated in vascular control during central volume depletion independent of such a serotonergic influence.

AB - The luminal diameter of the radial artery was followed by high frequency ultrasound during 50 degrees head-up tilt-induced central volume depletion in ten healthy subjects of whom six were tilted twice and pretreated with the serotonin receptor antagonist methysergide or placebo following a double-blind randomized design. Eight subjects without active treatment experienced presyncopal symptoms after 16-45 (mean 32 min). Central volume depletion was indicated by an increase in mean thoracic electrical impedance [from 31.5 (SEM 1.6) to 33.4 (SEM 1.7) omega; P < 0.05]. Cardiac output decreased [from 4.1 (SEM 0.3) to 2.2 (SEM 0.3) 1.min-1] and heart rate [HR, from 64 (SEM 3) to 100 (SEM 7) beats.min-1], mean arterial pressure (MAP, from 77 (SEM 4) to 89 (SEM 2) mmHg [10.3 (SEM 0.53 to 11.9 (SEM 0.27) kPa]) and total peripheral resistance (TPR, from 19 (SEM 2) to 34 (SEM 4) mmHg.min.1-1 [2.5 (SEM 0.27) to 4.5 (SEM 0.53) kPa.min.1-1]) increased; but with the appearance of presyncopal symptoms, HR, MAP and TPR were reduced to 65 (SEM 8) beats.min-1, 46 (SEM 4) mmHg [6.1 (SEM 0.53) kPa] and 18 (SEM 3) mmHg.min.1-1 [2.4 (SEM 0.4) kPa.min-1.1-1], respectively (P < 0.05). Vascular resistance was reflected in the arterial diameter which decreased from 2.42 (SEM 0.17) to 2.27 (SEM 0.14) mm during head-up tilt and increased to 2.71 (SEM 0.14) mm with the appearance of presyncopal symptoms (P < 0.05). Methysergide reduced the resting radial (15 +/- 2%) and temporal artery diameters (10 +/- 3%) (P < 0.05); however, it affected neither tilt-tolerance nor the central cardiovascular response to tilt. The results suggested a serotonergic influence on arterial tone at rest, and demonstrated that vessels as large as the radial artery participated in vascular control during central volume depletion independent of such a serotonergic influence.

KW - Adult

KW - Blood Pressure

KW - Blood Volume

KW - Cardiac Output

KW - Double-Blind Method

KW - Electric Impedance

KW - Female

KW - Heart Rate

KW - Humans

KW - Male

KW - Methysergide

KW - Placebos

KW - Posture

KW - Radial Artery

KW - Serotonin Antagonists

KW - Vascular Resistance

M3 - Journal article

C2 - 8789588

VL - 72

SP - 165

EP - 169

JO - European Journal of Applied Physiology and Occupational Physiology

JF - European Journal of Applied Physiology and Occupational Physiology

SN - 0301-5548

IS - 1-2

ER -

ID: 128984139