Effect of endogenous estrogen on blood flow through carotid arteries

Citation
J. Krejza et al., Effect of endogenous estrogen on blood flow through carotid arteries, STROKE, 32(1), 2001, pp. 30-36
Citations number
47
Categorie Soggetti
Neurology,"Cardiovascular & Hematology Research
Journal title
STROKE
ISSN journal
00392499 → ACNP
Volume
32
Issue
1
Year of publication
2001
Pages
30 - 36
Database
ISI
SICI code
0039-2499(200101)32:1<30:EOEEOB>2.0.ZU;2-Q
Abstract
Background and Purpose-Recent evidence suggests that physiological changes in the concentration of endogenous estrogens may influence stroke outcome. The purpose of this study was to determine a menstrual cycle-related profil e of blood flow through the carotid arteries and its correlation with estro gen concentration. Methods-The flow velocity and cross-sectional area of the common carotid ar tery, internal carotid artery (ICA), and external carotid artery (ECA) were measured with duplex Doppler sonography throughout the menstrual cycle in 14 healthy women. Concentration of plasma 17 beta -estradiol, progesterone, hematocrit, hemoglobin, and blood pressure were also determined. Results-In the follicular phase, the concentration of estrogen increased to reach a peak on day 14, whereas concentration of progesterone remained low . The mean and end-diastolic velocities in the ICA increased on average by 15% of their base values, along with increasing concentrations of estrogen (r=0.59 and 0.65, respectively). The profile of flow velocity changes in th is artery corresponded to the profile of estrogen concentration. In contras t to the ICA, flow velocities in the ECA decreased from their base value, r eaching their minimum in the luteal phase. The mean flow velocity in the co mmon carotid artery increased on day 14 by just 2% of its base value. The l umen of the carotid arteries was stable throughout the cycle. Hematocrit, h emoglobin, and systolic blood pressure also remained unchanged. Conclusions-Increased concentration of endogenous estrogen correlates with substantial augmentation of flow in the internal carotid artery. This promo tion of flow is caused mainly by decreased cerebrovascular resistance with consequent "stealing" of blood from the ECA.