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Menstrual cycle and oral contraceptives influence cerebrovascular dynamics during hypercapnia

Women experience fluctuating orthostatic intolerance during the menstrual cycle, suggesting sex hormones may influence cerebral blood flow. Young (aged 18–30) healthy women, either taking oral contraceptives (OC; n = 14) or not taking OC (NOC; n = 12), were administered hypercapnic gas (5%) for 5 mi...

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Autores principales: Pereira, Tania J., Wasef, Sara, Ivry, Ilana, Assadpour, Elnaz, Adeyinka, Baithat O., Edgell, Heather
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9277257/
https://www.ncbi.nlm.nih.gov/pubmed/35822289
http://dx.doi.org/10.14814/phy2.15373
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author Pereira, Tania J.
Wasef, Sara
Ivry, Ilana
Assadpour, Elnaz
Adeyinka, Baithat O.
Edgell, Heather
author_facet Pereira, Tania J.
Wasef, Sara
Ivry, Ilana
Assadpour, Elnaz
Adeyinka, Baithat O.
Edgell, Heather
author_sort Pereira, Tania J.
collection PubMed
description Women experience fluctuating orthostatic intolerance during the menstrual cycle, suggesting sex hormones may influence cerebral blood flow. Young (aged 18–30) healthy women, either taking oral contraceptives (OC; n = 14) or not taking OC (NOC; n = 12), were administered hypercapnic gas (5%) for 5 min in the low hormone (LH; placebo pill) and high hormone (HH; active pill) menstrual phases. Hemodynamic and cerebrovascular variables were continuously measured. Cerebral blood velocity changes were monitored using transcranial doppler ultrasound of the middle cerebral artery to determine cerebrovascular reactivity. Cerebral autoregulation was assessed using steady‐state analysis (static cerebral autoregulation) and transfer function analysis (dynamic cerebral autoregulation; dCA). In response to hypercapnia, menstrual phase did not influence static cardiovascular or cerebrovascular responses (all p > 0.07); however, OC users had a greater increase of mean middle cerebral artery blood velocity compared to NOC (NOC‐LH 12 ± 6 cm/s vs. NOC‐HH 16 ± 9 cm/s; OC‐LH 18 ± 5 cm/s vs. OC‐HH 17 ± 11 cm/s; p = 0.048). In all women, hypercapnia improved high frequency (HF) and very low frequency (VLF) cerebral autoregulation (decreased nGain; p = 0.002 and <0.001, respectively), whereas low frequency (LF) Phase decreased in NOC‐HH (p = 0.001) and OC‐LH (p = 0.004). Therefore, endogenous sex hormones reduce LF dCA during hypercapnia in the HH menstrual phase. In contrast, pharmaceutical sex hormones (OC use) have no acute influence (HH menstrual phase) yet elicit a chronic attenuation of LF dCA (LH menstrual phase) during hypercapnia.
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spelling pubmed-92772572022-07-15 Menstrual cycle and oral contraceptives influence cerebrovascular dynamics during hypercapnia Pereira, Tania J. Wasef, Sara Ivry, Ilana Assadpour, Elnaz Adeyinka, Baithat O. Edgell, Heather Physiol Rep Original Articles Women experience fluctuating orthostatic intolerance during the menstrual cycle, suggesting sex hormones may influence cerebral blood flow. Young (aged 18–30) healthy women, either taking oral contraceptives (OC; n = 14) or not taking OC (NOC; n = 12), were administered hypercapnic gas (5%) for 5 min in the low hormone (LH; placebo pill) and high hormone (HH; active pill) menstrual phases. Hemodynamic and cerebrovascular variables were continuously measured. Cerebral blood velocity changes were monitored using transcranial doppler ultrasound of the middle cerebral artery to determine cerebrovascular reactivity. Cerebral autoregulation was assessed using steady‐state analysis (static cerebral autoregulation) and transfer function analysis (dynamic cerebral autoregulation; dCA). In response to hypercapnia, menstrual phase did not influence static cardiovascular or cerebrovascular responses (all p > 0.07); however, OC users had a greater increase of mean middle cerebral artery blood velocity compared to NOC (NOC‐LH 12 ± 6 cm/s vs. NOC‐HH 16 ± 9 cm/s; OC‐LH 18 ± 5 cm/s vs. OC‐HH 17 ± 11 cm/s; p = 0.048). In all women, hypercapnia improved high frequency (HF) and very low frequency (VLF) cerebral autoregulation (decreased nGain; p = 0.002 and <0.001, respectively), whereas low frequency (LF) Phase decreased in NOC‐HH (p = 0.001) and OC‐LH (p = 0.004). Therefore, endogenous sex hormones reduce LF dCA during hypercapnia in the HH menstrual phase. In contrast, pharmaceutical sex hormones (OC use) have no acute influence (HH menstrual phase) yet elicit a chronic attenuation of LF dCA (LH menstrual phase) during hypercapnia. John Wiley and Sons Inc. 2022-07-12 /pmc/articles/PMC9277257/ /pubmed/35822289 http://dx.doi.org/10.14814/phy2.15373 Text en © 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Pereira, Tania J.
Wasef, Sara
Ivry, Ilana
Assadpour, Elnaz
Adeyinka, Baithat O.
Edgell, Heather
Menstrual cycle and oral contraceptives influence cerebrovascular dynamics during hypercapnia
title Menstrual cycle and oral contraceptives influence cerebrovascular dynamics during hypercapnia
title_full Menstrual cycle and oral contraceptives influence cerebrovascular dynamics during hypercapnia
title_fullStr Menstrual cycle and oral contraceptives influence cerebrovascular dynamics during hypercapnia
title_full_unstemmed Menstrual cycle and oral contraceptives influence cerebrovascular dynamics during hypercapnia
title_short Menstrual cycle and oral contraceptives influence cerebrovascular dynamics during hypercapnia
title_sort menstrual cycle and oral contraceptives influence cerebrovascular dynamics during hypercapnia
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9277257/
https://www.ncbi.nlm.nih.gov/pubmed/35822289
http://dx.doi.org/10.14814/phy2.15373
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