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Influence of menstrual cycle phase on the cerebrovascular response to hypoxia: role of cyclooxygenase (708.1)
Author(s) -
Peltonen Garrett,
Rosseau Cameron,
Harrell John,
Schrage William
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.708.1
Subject(s) - follicular phase , luteal phase , menstrual cycle , endocrinology , medicine , cyclooxygenase , hypoxia (environmental) , cerebral blood flow , estrogen , chemistry , hormone , biochemistry , organic chemistry , oxygen , enzyme
Menstrual phases influence resting cerebral blood flow (CBF), partially through cyclooxygenase (COX) mediated signaling. It is unknown if menstrual cycle hormone variations influence the CBF response to hypoxic stress. Compared to early follicular phase, we hypothesized females in early luteal phase would exhibit a larger, COX‐dependent, hypoxia‐mediated increase in CBF. We measured middle cerebral artery velocity (MCAv) with transcranial Doppler ultrasound in 4 healthy females (22 ± 3 yrs). Cerebral vascular conductance index (CVCi = MCAv*100/MABP) was calculated to normalize for potential differences in blood pressure. Females were studied twice each in early follicular (cycle day 1‐5) and late luteal (cycle day 12‐16) phases of the menstrual cycle, with and without COX inhibition (100 mg oral Indomethacin, Indo). Arterial O2 (SaO2) was reduced to 80% for 5 minutes while clamping end‐tidal CO2. On average, estrogen was higher (188 vs. 55 pg ml‐1) and progesterone was similar (790 vs. 603 pg ml‐1) during early luteal phase. Menstrual phase had no effect on basal CVCi (p=0.67) or the decrease in basal CVCi with Indo (p=0.45). Hypoxia increased CVCi (∆CVCi = 12 ± 1 cm s‐1 mmHg‐1; p<0.001), but the hypoxia‐induced ∆CVCi was not altered by menstrual phase (p=0.53) or Indo (p=0.873). These data suggest that menstrual phase does not alter basal or hypoxic CVCi and the role of COX is unchanged in either response. Grant Funding Source : NIH R01 HL105820 & AHA PRE7390038