Mechanisms of increase in cardiac output during acute weightlessness in humans

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Mechanisms of increase in cardiac output during acute weightlessness in humans. / Petersen, Lonnie G; Damgaard, Morten; Petersen, Johan Casper Grove; Norsk, Peter.

I: Journal of Applied Physiology, Bind 111, Nr. 2, 01.08.2011, s. 407-11.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Petersen, LG, Damgaard, M, Petersen, JCG & Norsk, P 2011, 'Mechanisms of increase in cardiac output during acute weightlessness in humans', Journal of Applied Physiology, bind 111, nr. 2, s. 407-11. https://doi.org/10.1152/japplphysiol.01188.2010

APA

Petersen, L. G., Damgaard, M., Petersen, J. C. G., & Norsk, P. (2011). Mechanisms of increase in cardiac output during acute weightlessness in humans. Journal of Applied Physiology, 111(2), 407-11. https://doi.org/10.1152/japplphysiol.01188.2010

Vancouver

Petersen LG, Damgaard M, Petersen JCG, Norsk P. Mechanisms of increase in cardiac output during acute weightlessness in humans. Journal of Applied Physiology. 2011 aug 1;111(2):407-11. https://doi.org/10.1152/japplphysiol.01188.2010

Author

Petersen, Lonnie G ; Damgaard, Morten ; Petersen, Johan Casper Grove ; Norsk, Peter. / Mechanisms of increase in cardiac output during acute weightlessness in humans. I: Journal of Applied Physiology. 2011 ; Bind 111, Nr. 2. s. 407-11.

Bibtex

@article{baf4a3ca1de746f485aa63c8b612da33,
title = "Mechanisms of increase in cardiac output during acute weightlessness in humans",
abstract = "Based on previous water immersion results, we tested the hypothesis that the acute 0-G-induced increase in cardiac output (CO) is primarily caused by redistribution of blood from the vasculature above the legs to the cardiopulmonary circulation. In seated subjects (n = 8), 20 s of 0 G induced by parabolic flight increased CO by 1.7 ± 0.4 l/min (P <0.001). This increase was diminished to 0.8 ± 0.4 l/min (P = 0.028), when venous return from the legs was prevented by bilateral venous thigh-cuff inflation (CI) of 60 mmHg. Because the increase in stroke volume during 0 G was unaffected by CI, the lesser increase in CO during 0 G + CI was entirely caused by a lower heart rate (HR). Thus blood from vascular beds above the legs in seated subjects can alone account for some 50{\%} of the increase in CO during acute 0 G. The remaining increase in CO is caused by a higher HR, of which the origin of blood is unresolved. In supine subjects, CO increased from 7.1 ± 0.7 to 7.9 ± 0.8 l/min (P = 0.037) when entering 0 G, which was solely caused by an increase in HR, because stroke volume was unaffected. In conclusion, blood originating from vascular beds above the legs can alone account for one-half of the increase in CO during acute 0 G in seated humans. A Bainbridge-like reflex could be the mechanism for the HR-induced increase in CO during 0 G in particular in supine subjects.",
author = "Petersen, {Lonnie G} and Morten Damgaard and Petersen, {Johan Casper Grove} and Peter Norsk",
year = "2011",
month = "8",
day = "1",
doi = "10.1152/japplphysiol.01188.2010",
language = "English",
volume = "111",
pages = "407--11",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "2",

}

RIS

TY - JOUR

T1 - Mechanisms of increase in cardiac output during acute weightlessness in humans

AU - Petersen, Lonnie G

AU - Damgaard, Morten

AU - Petersen, Johan Casper Grove

AU - Norsk, Peter

PY - 2011/8/1

Y1 - 2011/8/1

N2 - Based on previous water immersion results, we tested the hypothesis that the acute 0-G-induced increase in cardiac output (CO) is primarily caused by redistribution of blood from the vasculature above the legs to the cardiopulmonary circulation. In seated subjects (n = 8), 20 s of 0 G induced by parabolic flight increased CO by 1.7 ± 0.4 l/min (P <0.001). This increase was diminished to 0.8 ± 0.4 l/min (P = 0.028), when venous return from the legs was prevented by bilateral venous thigh-cuff inflation (CI) of 60 mmHg. Because the increase in stroke volume during 0 G was unaffected by CI, the lesser increase in CO during 0 G + CI was entirely caused by a lower heart rate (HR). Thus blood from vascular beds above the legs in seated subjects can alone account for some 50% of the increase in CO during acute 0 G. The remaining increase in CO is caused by a higher HR, of which the origin of blood is unresolved. In supine subjects, CO increased from 7.1 ± 0.7 to 7.9 ± 0.8 l/min (P = 0.037) when entering 0 G, which was solely caused by an increase in HR, because stroke volume was unaffected. In conclusion, blood originating from vascular beds above the legs can alone account for one-half of the increase in CO during acute 0 G in seated humans. A Bainbridge-like reflex could be the mechanism for the HR-induced increase in CO during 0 G in particular in supine subjects.

AB - Based on previous water immersion results, we tested the hypothesis that the acute 0-G-induced increase in cardiac output (CO) is primarily caused by redistribution of blood from the vasculature above the legs to the cardiopulmonary circulation. In seated subjects (n = 8), 20 s of 0 G induced by parabolic flight increased CO by 1.7 ± 0.4 l/min (P <0.001). This increase was diminished to 0.8 ± 0.4 l/min (P = 0.028), when venous return from the legs was prevented by bilateral venous thigh-cuff inflation (CI) of 60 mmHg. Because the increase in stroke volume during 0 G was unaffected by CI, the lesser increase in CO during 0 G + CI was entirely caused by a lower heart rate (HR). Thus blood from vascular beds above the legs in seated subjects can alone account for some 50% of the increase in CO during acute 0 G. The remaining increase in CO is caused by a higher HR, of which the origin of blood is unresolved. In supine subjects, CO increased from 7.1 ± 0.7 to 7.9 ± 0.8 l/min (P = 0.037) when entering 0 G, which was solely caused by an increase in HR, because stroke volume was unaffected. In conclusion, blood originating from vascular beds above the legs can alone account for one-half of the increase in CO during acute 0 G in seated humans. A Bainbridge-like reflex could be the mechanism for the HR-induced increase in CO during 0 G in particular in supine subjects.

U2 - 10.1152/japplphysiol.01188.2010

DO - 10.1152/japplphysiol.01188.2010

M3 - Journal article

VL - 111

SP - 407

EP - 411

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 2

ER -

ID: 33967681