atrial-natriuretic-factor and Fetal-Hypoxia

The purpose of this study was to observe endocrinological responses of veno-arterial and veno-venous extracorporeal membrane oxygenation (V-A and V-V ECMO) to support fetal oxygenation in utero.. An ECMO system with a centrifugal pump was applied to six chronically instrumented fetal lambs, at 126-134 days of gestation. Blood was obtained through a double-lumen catheter inserted into the right atrium. After oxygenation, the blood was returned through a single-lumen catheter into either the carotid artery (veno-arterial; V-A ECMO) or the right atrium (V-V ECMO). After fetal hypoxia had been experimentally produced, V-A ECMO or V-V ECMO was instituted to maintain fetal oxygenation. We compared fetal blood gases and concentrations of atrial natriuretic peptide (ANP), epinephrine and norepinephrine with both routes of ECMO.. Fetal carotid artery pH did not change during hypoxemia, but decreased after instituting V-A ECMO and V-V ECMO. After instituting V-A ECMO or V-V ECMO for 30 min, oxygen partial pressure (pO2) in the fetal cranial carotid artery recovered from the hypoxic level. The ANP concentration in V-V ECMO was significantly lower than that in V-A ECMO. Fetal serum epinephrine and norepinephrine concentrations significantly increased in association with hypoxic stimulation. There was a further increase in fetal serum epinephrine concentration after instituting V-A ECMO. No significant difference in concentration was found after instituting V-V ECMO from that of after the institution of V-A ECMO.. This study suggested that V-V ECMO may possibly be less invasive than V-A ECMO for fetal heart, because ANP, a cardiac distress index, was lower in V-V ECMO than in V-A ECMO.

Topics: Animals; Atrial Natriuretic Factor; Blood Gas Analysis; Epinephrine; Extracorporeal Membrane Oxygenation; Fetal Heart; Fetal Hypoxia; Fetus; Norepinephrine; Oxygen; Sheep, Domestic

This study investigated the maturational change in the atrial natriuretic factor response to hypoxia in ovine fetuses and the role of the autonomic nervous system and arginine vasopressin in modulating this response.. Chronically catheterized ovine fetuses from 110 to 135 days' gestation were subjected to 30 minutes of hypoxia. The fetuses were either intact, treated with hexamethonium to block the autonomic nervous system, or treated with a pressor antagonist of arginine vasopressin.. Hypoxia elevated plasma atrial natriuretic factor levels by 1635 +/- 265 pg/ml in immature fetuses; this response was greater than the increase of 748 +/- 189 pg/ml in mature fetuses (p < 0.0001). Blockade of the autonomic nervous system reduced the atrial natriuretic factor response and suppressed the vascular pressure changes to hypoxia in immature but not in mature fetuses. A vasopressin pressor antagonist suppressed the atrial natriuretic factor but not vascular pressure responses to hypoxia in mature fetuses.. This study demonstrates that the immature fetus manifested a greater atrial natriuretic factor response to hypoxia than did the mature fetus. This enhanced response appeared to be dependent on the modulatory effects of the autonomic nervous system on vascular pressures during hypoxia. In addition, arginine vasopressin appeared to augment the atrial natriuretic factor response to hypoxia in the mature fetus independent of vascular pressure changes.

Topics: Animals; Arginine Vasopressin; Atrial Natriuretic Factor; Autonomic Nervous System; Blood Gas Analysis; Blood Pressure; Female; Fetal Blood; Fetal Hypoxia; Fetal Organ Maturity; Gestational Age; Heart Rate, Fetal; Pregnancy; Sheep