title: Effect of endogenous estrogen on blood flow through carotid arteries.
abstract: OBJECTIVE
  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 profile of blood flow through the carotid arteries and its correlation with estrogen concentration.
  
  
  METHODS
  The flow velocity and cross-sectional area of the common carotid artery, 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 17beta-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 this artery corresponded to the profile of estrogen concentration. In contrast to the ICA, flow velocities in the ECA decreased from their base value, reaching their minimum in the luteal phase. The mean flow velocity in the common carotid artery increased on day 14 by just 2% of its base value. The lumen of the carotid arteries was stable throughout the cycle. Hematocrit, hemoglobin, 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 promotion of flow is caused mainly by decreased cerebrovascular resistance with consequent "stealing" of blood from the ECA.
authors.affiliation: Department of Radiology, Bialystok Medical Academy, Bialystok, Poland. jkrejza@cksr.ac.bialystok.pl
authors.forename: J
authors.initials: J
authors.lastname: Krejza
authors.forename: Z
authors.initials: Z
authors.lastname: Mariak
authors.forename: M
authors.initials: M
authors.lastname: Huba
authors.forename: S
authors.initials: S
authors.lastname: Wolczynski
authors.forename: J
authors.initials: J
authors.lastname: Lewko
mesh_terms: D000328:Adult; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000502:physiology; D004958:Estradiol / Q000097:blood; D004967:Estrogens / Q000097:blood* / Q000494:pharmacology; D005260:Female; D005498:Follicular Phase / Q000502:physiology; D006400:Hematocrit; D006454:Hemoglobins / Q000032:analysis; D006801:Humans; D008183:Luteal Phase / Q000502:physiology; D008597:Menstrual Cycle / Q000097:blood*; D011374:Progesterone / Q000097:blood; D011446:Prospective Studies; D018616:Ultrasonography, Doppler, Duplex; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology
chemical_list: D004967:Estrogens; D006454:Hemoglobins; D011374:Progesterone; D004958:Estradiol