Vol. 275, Issue 1, H57-H64, July 1998
17
-Estradiol effect on critical cardiac output with
reduction of cardiac output in oophorectomized sheep
Wayne
Evans1,3,
Terrance M.
Phernetton1, and
Ronald R.
Magness1,2
1 Perinatal Research
Laboratories, Department of Obstetrics and Gynecology and
2 Department of Meat and Animal
Sciences, University of Wisconsin Medical School, Madison 53792; and
3 Milwaukee Clinical Campus, Sinai
Samaritan Medical Center, Milwaukee, Wisconsin 53201-0342
Acute administration
of 17
-estradiol (E2) leads
to increases in cardiac output, oxygen delivery, and oxygen consumption and increases the critical cardiac output in the nonpregnant sheep. We
sought to determine whether the lack of a critical cardiac output or
flow-dependent oxygen consumption during states of low cardiac output
in late gestation can be reproduced in nonpregnant sheep treated with
estrogen. We studied five nonpregnant oophorectomized sheep in a
randomized crossover design by placing catheters in the pulmonary
artery, the right atrium, and the descending aorta. Three experiments
were randomly performed on each sheep 3 to 5 days apart:
1) without estrogen or vehicle,
2) 2-3 h after intravenous administration of vehicle, and 3)
2-3 h after intravenous E2 (3 µg/kg). Cardiac output was gradually reduced while hemodynamic, cardiorespiratory, acid-base, and metabolic variables were
simultaneously evaluated. There was a 70% increase in cardiac output
in animals given E2 compared
with that in the same animals given either vehicle or nothing (194.0 ± 13.0, 120.0 ± 14.5, and 114.0 ± 16.2 ml · min
1 · kg1,
respectively; P < 0.05). Oxygen
consumption was twofold higher in the
E2 series compared with that in
the no-treatment and vehicle series (10.01 ± 1.3, 6.04 ± 0.77, and 4.52 ± 0.42 ml
O2 · min1 · kg1,
respectively; P < 0.05). Tissue
oxygen extraction was unaltered by estrogen. However, tissue oxygen
extraction at the critical cardiac output was lower in the estradiol
group. In relation to oxygen consumption, all three groups demonstrated
a critical cardiac output when cardiac output was gradually reduced.
However, the level of critical cardiac output was significantly higher
in the E2 group (68.4 ± 2.4, 42.8 ± 2.6, and 46.2 ± 2.6 ml · min1 · kg1,
respectively; P < 0.05). We conclude
that E2 exhibits increases in
systemic tissue blood flow and oxygen consumption. Animals given
E2 show increases in critical
cardiac output and impairment of tissue oxygen extraction at critical
cardiac output, which leads to development of flow-dependent oxygen
consumption at higher cardiac outputs than in the control animals.
oxygen delivery; oxygen consumption; tissue oxygen extraction; lactate; glucose
