• Reller, Mark (PI)

Project: Research project

Project Details


Hypoxemia is a major problem with significant adverse effects on
both the fetus and the newborn infant. The accepted experimental
model for the investigation of fetal hypoxemia has been to reduce
the inspired oxygen concentration in the maternal ewe. Using this
model, fetal hypoxemia is frequently associated with reduced
cardiac output due to reduced stroke volume and arterial
hypertension. Previous investigations have demonstrated that
myocardial oxygen delivery increases during fetal hypoxemia
primarily by increased coronary blood flow accomplished by coronary
vasodilation. A proposed mechanism for the reduction in combined
ventricular output in the fetus with hypoxemia is that stroke
volume drops due to an associated increase in arterial pressure. Previous investigations from this laboratory have demonstrated that
the two fetal ventricles have distinctly different sensitivities
to arterial pressure--that is, increases in arterial pressure
result in significant reductions in right ventricular stroke
volume, while left ventricular stroke volume remains constant.
Hypoxemia, when associated with fetal arterial hypertension would,
by itself, be expected to produce a substantial reduction in right
ventricular output. The purpose of this investigation is to determine the mechanism(s)
for the reduction in fetal cardiac output with hypoxemia. The plan
is to test the hypotheses that: 1) stroke volume sensitivity to
increased arterial pressure, or 2) inadequate coronary blood flow
with hypoxemia and increased arterial pressure, reduces cardiac
output. To accomplish these goals, we plan the following specific
aims in the chronically Instrumented near term fetal lamb: a)
generate biventricular function curves before and during fetal
hypoxemia, and during hypoxemia after normalization of arterial
pressure, b) generate biventricular stroke volume-arterial pressure
relationship curves during hypoxemia, c) determine the arterial
pressure at which myocardial blood flow limits biventricular
performance during normoxemia and during hypoxemia. These specific
aims integrate the principal investigator's long-term interest and
commitment to the understanding of the pathophysiology of fetal and
neonatal hypoxemia with a laboratory possessing expertise in fetal
hemodynamics and ventricular function.
Effective start/end date9/30/888/31/91


  • National Institutes of Health


  • Medicine(all)


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