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Departments of 1 Physiology and Pharmacology and Medicine (Cardiology) and 3 Pediatrics (Pediatric Cardiology) and the 2 Congenital Heart Research Center, Oregon Health Sciences University, Portland, Oregon 97201
The two
ventricles of the fetal sheep heart have anatomic and biochemical
differences that account for their differing functional capabilities
and blood flows. Coronary flows to both ventricles have been measured
using radiolabeled microspheres [or left ventricular (LV) flow,
by Doppler sensor on the circumflex coronary artery] during
experiments of pressure loading and chronic and acute hypoxemia. Blood
flow to the left ventricle with its lower wall tension is about
two-thirds the flow per gram compared with the right ventricle (RV).
Acute systolic pressure loading of the RV to its maximal work
capability stimulates flow to double (from ~250 to 500 ml · min
1 · 100 g
1), but to a level less
than stimulated by adenosine (750 ml · min
1 · 100 g
1). At all RV work
loads, LV flow remains at two-thirds RV flow. Resting myocardial flow
levels in fetuses that have been chronically hypoxemic are similar to
maximal adenosine-stimulated flows of normal fetal sheep. This flow
augmentation is evidently due to vascular remodeling because a normal
"flow reserve" of ~500
ml · min
1 · 100 g
1 during adenosine
administration remains. Acute hypoxemia stimulates myocardial flow to
extraordinary levels (>1.5
l · min
1 · 100 g
1), levels larger than can
be obtained with chemical dilation alone. LV flows do not exceed
adenosine-stimulated flows when nitric oxide synthase is antagonized.
We conclude 1) fetal RV coronary flow increases with RV work but to levels less than during adenosine stimulation; 2) the fetal heart is
designed to accommodate extremely high flows in response to acute
hypoxemia, partially through large production of nitric oxide; and
3) the fetal coronary tree is dramatically remodeled in response to chronic hypoxemia.
fetal heart; nitric oxide; adenosine; law of Laplace; fetal hypoxemia; wall stress; heart ventricle; coronary remodeling
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