1. Postural vasoconstriction in the foot was examined in 15 women during the menstrual, follicular and luteal phases of the menstrual cycle, and in 13 age-matched men on two separate occasions, in a constant-temperature environment (22°C).
2. Skin blood flow was measured using laser Doppler flowmetry with the subject lying down, first with the foot maintained at heart level, then with the foot lowered passively 50 cm below the heart. In six of the women, at the time of experiment, serum oestradiol and progesterone were determined by radioimmunoassay. In four women and three men, foot swelling rate was also measured in the dependent foot using a strain gauge plethysmograph in addition to the postural changes in flow. At each visit, in all subjects, arterial blood pressure, heart rate, body temperature, foot skin temperature and body weight were also recorded.
3. The men showed no significant changes in all the variables assessed. In contrast, in women during the luteal phase diastolic and mean arterial pressures were significantly reduced, whereas heart rate, body temperature, foot skin temperature and body weight were significantly increased, as compared with the follicular and menstrual phases of the cycle.
4. During the follicular phase, when oestradiol concentration was high, there were significant reductions in dependent flow and foot swelling rate associated with a significantly augmented postural fall in flow, whereas during the luteal phase, when both oestradiol and progesterone levels were high, there were significant increases in dependent flow and foot swelling rate associated with a significantly impaired postural fall in flow. Four women who reported premenstrual ankle oedema showed significantly higher flow values during the luteal phase than the rest of women.
5. These results confirm the modulating influence of female sex hormones on peripheral blood flow and vascular tone. The partially impaired postural vasoconstrictor response during the luteal phase of the cycle might be partly implicated in the pathogenesis of premenstrual oedema in some women.