Coronary flow regulation in the fetal sheep

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Abstract

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 1·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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume277
Issue number5 46-5
StatePublished - Nov 1999

Fingerprint

Heart Ventricles
Sheep
Adenosine
Fetal Heart
Third Ventricle
Workload
Microspheres
Nitric Oxide Synthase
Dilatation
Coronary Vessels
Nitric Oxide
Fetus
Blood Pressure
Pressure
Hypoxia

Keywords

  • Adenosine
  • Coronary remodeling
  • Fetal heart
  • Fetal hypoxemia
  • Heart ventricle
  • Law of Laplace
  • Nitric oxide
  • Wall stress

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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abstract = "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 1·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.",
keywords = "Adenosine, Coronary remodeling, Fetal heart, Fetal hypoxemia, Heart ventricle, Law of Laplace, Nitric oxide, Wall stress",
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AU - Thornburg, Kent

AU - Reller, Mark

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N2 - 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 1·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.

AB - 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 1·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.

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