Reproductive hormone-mediated thermoregulatory control shift is not blocked by acute ibuprofen

N. Charkoudian, J. M. Johnson

Research output: Contribution to journalArticlepeer-review

Abstract

We hypothesized that the thermoregulatory control shift seen with elevated progesterone and estrogen is a central, prostaglandin E2-mediated shift similar to that seen in a fever. To test this possibility, we conducted heat stress experiments in resting women in two phases of oral contraceptive use with and without acute ibuprofen (IBP, 800 mg): after three weeks of hormone pills (high hormone phase, HH; with IBP, HHi) and after one week of placebo pills (low hormone phase, LH; with IBP, LHi). Skin blood flow was monitored by laser Doppler flowmetry and sweating by capacitance hygrometry. Pre-heat stress resting internal temperature (Tor), and the Tor thresholds for cutaneous vasodilation and sweating were higher in HH (see table, all p<0.05). None of the shifts was affected by IBP (p>0.1).HH LHi HHi Tor (rest) 36.72±0.07 36.89±0.06 36.62±0.08 36.87±0.05 dilation thr. 36.86±0.07 37.15±0.09 36.78±0.08 37.07±0.05 sweating thr. 36.92±0.09 37.19±0.09 36.85±0.07 37.21±0.06 That the threshold shifts were not affected by ibuprofen suggests that the threshold shifts with high progesterone and estrogen occur via a mechanism that does not include prostaglandins.

Original languageEnglish (US)
Pages (from-to)A959
JournalFASEB Journal
Volume12
Issue number5
StatePublished - Mar 20 1998

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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