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-estradiol
1 Department of Obstetrics and
Gynecology,
Prolonged
17
-estradiol (E2
) infusion
decreases mean arterial pressure (MAP) and systemic vascular resistance
(SVR) while increasing heart rate (HR) and cardiac output (CO). It is
unclear, however, which systemic vascular beds show increases in
perfusion. The purpose of this study was to determine which
reproductive and nonreproductive vascular beds exhibit alterations in
vascular resistance and blood flow during prolonged
E2
infusion. Nonpregnant, ovariectomized sheep received either vehicle
(n = 6) or
E2
(5 µg/kg iv bolus followed
by 6 µg/kg over 24 h for 10 days; n = 9), and blood flow distribution was evaluated using radiolabeled microspheres at control and 120 min and 3, 6, 8, and 10 days of infusion. During E2
infusion
MAP (87 ± 5 mmHg; mean ± SE) decreased 3-9% and HR (83 ± 5 beats/min) increased 4-31%. The combined baseline (control) perfusion to the uterus, broad ligament, oviducts, cervix, vagina, and mammary gland (reproductive blood flows) was 49 ± 9 ml/min; at 120 min, E2
increased flow (P < 0.001) to 605 ± 74 ml/min (1,263%) and it remained elevated, but at a reduced rate, on day 3 (218 ± 44 ml/min;
399%), day
6 (144 ± 23; 217%), day 8 (181 ± 19; 321%), and day
10 (204 ± 48; 454%), accounting for only 3-17% of the
E2
-induced increase in CO.
During this E2
treatment, there
also were significant decreases in vascular resistances leading to
increases (P < 0.05) in blood flows
to several nonreproductive (systemic) vascular beds including skin (32-113%), coronary (32-190%), skeletal muscle
(25-133%), brain (21-292%), bladder (128-524%),
spleen (87-180%), and pancreas (35-137%) vascular beds.
Responses of these combined nonreproductive blood flows represent the
major percentage (21-67%) of the
E2
-induced increase in CO.
Vehicle infusion was without effect. We conclude that prolonged
E2
infusion increases
reproductive and nonreproductive tissue blood flows. The latter appears
to principally be responsible for the observed rise in CO and decrease
in SVR.
blood pressure; cardiac output; vascular resistance; hormone replacement therapy; pregnancy; estrogen; ovine model
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