HEMODYNAMIC-EFFECTS ON BRACHIAL-ARTERY OF ESTRADIOL AND PROGESTERONE REPLACEMENT IN WOMEN WITH INACTIVE OVARIES

To determine the effects of female hormones on peripheral vasculature we studied the brachial artery circulation. Nine young women (27-37 yr s) having inactive ovaries received transdermal estradiol (E2) 0.1 - 0 .4 mg/d) and vaginal progesteron (P) (300 mg/d) to duplicate the menst rual cycle levels of E2 and P. Brachial artery diameter, blood velocit y and flow were measured by bidimensional pulsed Doppler in basal cond itions, and during hand exclusion by a cuff inflated at suprasystolic pressure. Vascular resistance was calculated by the ratio of mean bloo d pressure over mean flow Measurements were obtained before hormonothe rapy (d0), on day 14 (d14, after E2), and on day 28 (d28, after E2 and P). The increase of brachial artery diameter began at d14 (3.73 +/- 0 .12 mm, vs 3.66 +/- 0.11 mm ; NS) to become significant at d28 (3.91 /- 0.10 mm, p < 0.05). Blood velocity and flow increased at d28 (4.78 +/- 0.55 cm/s, vs 3.55 +/- 0.65 cm/s; P < 0.05 and 35.2 +/- 5.2 ml/mn vs 22.2 +/- 3.6 ml/mn, P < 0.05 respectively). No change was noted in mean blood pressure. The decrease of resistance began at d14, in order to be significant at d28 (158 +/- 17 mmHg/ml/s at d0 vs 263 +/- 31 mm Hg/ml /s at d28 ; P < 0.05). Brachial vasoconstriction during hand exc lusion, in response to low flow state disappeared at d14 with estradio l. In conclusion, in women deprived of ovarian function, physiological E2 and P replacement vasodilates small and large arteries, whereas E2 alone attenuates the large artery vasoconstriction in acute response to low flow state. Thus, there is a dissociation between arterial vaso dilation which requires the association of E2 and P and the endotheliu m mediation vasoactivity which seems to be dependent of E2 alone.