Nitric oxide is an important determinant of coronary flow at rest
and during hypoxemic stress in the fetal lamb.
Reller, Mark D, Mike A Burson, Jamie L Lohr, Mark J Morton, Kent L
Thornburg.
Departments of Pediatrics (Cardiology), Medicine (Cardiology),
Physiology, and the University Congenital Heart Research Center;
Oregon Health Sciences University, Portland, Oregon, 97201
APStracts 2:0378H, 1995.
Fourteen fetal lambs were instrumented with atrial, coronary sinus,
and arterial catheters, and a proximal left circumflex coronary
artery Doppler probe and were studied at a mean gestational age of
130 + 3 (S.D.) days, 7 + 2 days after surgery. Myocardial blood flow
was assessed using 15 micron microspheres and Doppler flow
velocities. In 11 fetuses, the maximal myocardial flow response to
left atrial adenosine infusion was 802 + 215 ml/minute/100gm, 3.5
-fold greater than baseline flow. Acute fetal hypoxemia in 6 fetuses
to a PaO2 of 8.8 + 0.8 mmHg and an arterial content (CaO2 ) of 1.7 +
0.2 ml/dl was not associated with significant change in coronary
perfusion pressure, yet left ventricular myocardial flow increased to
1020 + 198 ml/minute/100gm, a value significantly greater than that
seen with adenosine (p < 0.05). Left atrial N-nitro-L-arginine
(L-NA), a competitive inhibitor of nitric oxide synthase (NOS), was
infused at a dosage of 1 mg/kg/minute for 60 minutes in 10 fetuses.
Although L-NA was associated with a significant increase in arterial
pressure, left ventricular myocardial flow decreased (162 + 79
ml/minute/100gm) as did myocardial oxygen consumption (p <
0.05). Acute hypoxemia in 5 of the fetuses who received L-NA was
associated with significant further increases in systemic arterial
pressure, however, left ventricular myocardial flow was only 771 +
237 ml/minute/100gm, a value similar to that seen with adenosine and
75% of that seen with acute hypoxemia alone. We conclude that nitric
oxide plays an important role in the regulation of fetal myocardial
flow during basal conditions as well as in the exuberant vasodilatory
response associated with acute hypoxemic stress.
Received 23 September 1994; accepted in final form 20 June 1995.
APS Manuscript Number H858-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 15 September 1995.