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Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284-7756
We tested the
hypothesis that the shift in the cutaneous vasodilator response to
hyperthermia seen with elevated female reproductive hormones is a
prostaglandin-dependent resetting of thermoregulation to higher
internal temperatures, similar to that seen in the febrile response to
bacterial infection. Using water-perfused suits to control body
temperature, we conducted heat stress experiments in resting women
under conditions of low and high progesterone and estrogen and repeated
these experiments after an acute dose of ibuprofen (800 mg). In six
women the hormones were exogenous (oral contraceptives); three women
had regular menstrual cycles and were tested in the early follicular
and midluteal phases. Resting oral temperature
(Tor) was significantly elevated
with high hormone status (P < 0.05);
this was not affected by ibuprofen treatment
(P > 0.2). The
Tor threshold for cutaneous
vasodilation was significantly increased by high hormone status (+0.27 ± 0.07°C, P < 0.02); the
shift was not affected by ibuprofen treatment (with ibuprofen: +0.29 ± 0.08°C, P > 0.2 vs.
control experiments). The Tor
threshold for sweating was similarly increased by high hormone status
(+0.22 ± 0.05°C, P < 0.05);
this shift was not influenced by ibuprofen (with ibuprofen: +0.35 ± 0.05, P > 0.1 vs. control experiments). Thus the shift in thermoregulatory control of skin blood
flow and sweating mediated by female reproductive steroids is not
sensitive to ibuprofen; it therefore appears that this shift is
independent of prostaglandins.
skin blood flow; estrogen; progesterone; heat stress; active vasodilation; sweating; human; temperature regulation
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