Nitric oxide is an important determinant of coronary flow at rest and during hypoxemic stress in fetal lambs

Mark Reller, M. A. Burson, J. L. Lohr, M. J. Morton, Kent Thornburg

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Abstract

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 (SD) days, 7 ± 2 days after surgery. Myocardial blood flow was assessed using 15-μm microspheres and Doppler flow velocities. In 11 fetuses, the maximal myocardial flow response to left atrial adenosine infusion was 802 ± 215 ml · min-1 · 100 g-1, 3.5-fold greater than baseline flow. Acute fetal hypoxemia in six fetuses to an arterial PO2 of 8.8 ± 0.8 mmHg and an arterial O2 content (Ca(O2)) of 1.7 ± 0.2 ml/dl was not associated with significant change in coronary perfusion pressure; yet left ventricular myocardial flow increased to 1,020 ± 198 ml · min-1 · 100 g-1, a value significantly greater than that seen with adenosine (P <0.05). Left atrial N(ω)-nitro-L-arginine (L-NNA), a competitive inhibitor of nitric oxide synthase (NOS), was infused at a dosage of ~1 mg · kg-1 · min-1 for 60 min in 10 fetuses. Although L-NNA was associated with a significant increase in arterial pressure, left ventricular myocardial flow decreased (162 ± 79 ml · min-1 · 100 g-1) as did myocardial O2 consumption (P <0.05). Acute hypoxemia in five fetuses that received L-NNA was associated with significant further increases in systemic arterial pressure; however, left ventricular myocardial flow was only 771 ± 237 ml · min-1 · 100 g-1, 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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume269
Issue number6 38-6
StatePublished - 1995

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Nitric Oxide
Fetus
Adenosine
Arterial Pressure
Coronary Sinus
Ambulatory Surgical Procedures
Microspheres
Nitric Oxide Synthase
Gestational Age
Arginine
Coronary Vessels
Catheters
Perfusion
Pressure
Hypoxia

Keywords

  • coronary Doppler flow velocity
  • fetal myocardial blood flow
  • radiolabeled microsphere technique

ASJC Scopus subject areas

  • Physiology

Cite this

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title = "Nitric oxide is an important determinant of coronary flow at rest and during hypoxemic stress in fetal lambs",
abstract = "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 (SD) days, 7 ± 2 days after surgery. Myocardial blood flow was assessed using 15-μm microspheres and Doppler flow velocities. In 11 fetuses, the maximal myocardial flow response to left atrial adenosine infusion was 802 ± 215 ml · min-1 · 100 g-1, 3.5-fold greater than baseline flow. Acute fetal hypoxemia in six fetuses to an arterial PO2 of 8.8 ± 0.8 mmHg and an arterial O2 content (Ca(O2)) of 1.7 ± 0.2 ml/dl was not associated with significant change in coronary perfusion pressure; yet left ventricular myocardial flow increased to 1,020 ± 198 ml · min-1 · 100 g-1, a value significantly greater than that seen with adenosine (P <0.05). Left atrial N(ω)-nitro-L-arginine (L-NNA), a competitive inhibitor of nitric oxide synthase (NOS), was infused at a dosage of ~1 mg · kg-1 · min-1 for 60 min in 10 fetuses. Although L-NNA was associated with a significant increase in arterial pressure, left ventricular myocardial flow decreased (162 ± 79 ml · min-1 · 100 g-1) as did myocardial O2 consumption (P <0.05). Acute hypoxemia in five fetuses that received L-NNA was associated with significant further increases in systemic arterial pressure; however, left ventricular myocardial flow was only 771 ± 237 ml · min-1 · 100 g-1, 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.",
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T1 - Nitric oxide is an important determinant of coronary flow at rest and during hypoxemic stress in fetal lambs

AU - Reller, Mark

AU - Burson, M. A.

AU - Lohr, J. L.

AU - Morton, M. J.

AU - Thornburg, Kent

PY - 1995

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N2 - 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 (SD) days, 7 ± 2 days after surgery. Myocardial blood flow was assessed using 15-μm microspheres and Doppler flow velocities. In 11 fetuses, the maximal myocardial flow response to left atrial adenosine infusion was 802 ± 215 ml · min-1 · 100 g-1, 3.5-fold greater than baseline flow. Acute fetal hypoxemia in six fetuses to an arterial PO2 of 8.8 ± 0.8 mmHg and an arterial O2 content (Ca(O2)) of 1.7 ± 0.2 ml/dl was not associated with significant change in coronary perfusion pressure; yet left ventricular myocardial flow increased to 1,020 ± 198 ml · min-1 · 100 g-1, a value significantly greater than that seen with adenosine (P <0.05). Left atrial N(ω)-nitro-L-arginine (L-NNA), a competitive inhibitor of nitric oxide synthase (NOS), was infused at a dosage of ~1 mg · kg-1 · min-1 for 60 min in 10 fetuses. Although L-NNA was associated with a significant increase in arterial pressure, left ventricular myocardial flow decreased (162 ± 79 ml · min-1 · 100 g-1) as did myocardial O2 consumption (P <0.05). Acute hypoxemia in five fetuses that received L-NNA was associated with significant further increases in systemic arterial pressure; however, left ventricular myocardial flow was only 771 ± 237 ml · min-1 · 100 g-1, 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.

AB - 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 (SD) days, 7 ± 2 days after surgery. Myocardial blood flow was assessed using 15-μm microspheres and Doppler flow velocities. In 11 fetuses, the maximal myocardial flow response to left atrial adenosine infusion was 802 ± 215 ml · min-1 · 100 g-1, 3.5-fold greater than baseline flow. Acute fetal hypoxemia in six fetuses to an arterial PO2 of 8.8 ± 0.8 mmHg and an arterial O2 content (Ca(O2)) of 1.7 ± 0.2 ml/dl was not associated with significant change in coronary perfusion pressure; yet left ventricular myocardial flow increased to 1,020 ± 198 ml · min-1 · 100 g-1, a value significantly greater than that seen with adenosine (P <0.05). Left atrial N(ω)-nitro-L-arginine (L-NNA), a competitive inhibitor of nitric oxide synthase (NOS), was infused at a dosage of ~1 mg · kg-1 · min-1 for 60 min in 10 fetuses. Although L-NNA was associated with a significant increase in arterial pressure, left ventricular myocardial flow decreased (162 ± 79 ml · min-1 · 100 g-1) as did myocardial O2 consumption (P <0.05). Acute hypoxemia in five fetuses that received L-NNA was associated with significant further increases in systemic arterial pressure; however, left ventricular myocardial flow was only 771 ± 237 ml · min-1 · 100 g-1, 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.

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