Abstract

A drop in arterial oxygen content activates fetal chemoreflex including an increase in sympathetic activity leading to peripheralvasoconstriction and redistribution of bloodflow to protect the brain, myocardium, and adrenal glands. By using a chronicallyinstrumented fetal sheep model with intact placental circulation at near-term gestation, we investigated the relationship betweenperipheral chemoreflex activation induced by hypoxemia and central hemodynamics. A total of 17 Åland landrace sheep fetusesat 115–128/145 gestational days were instrumented. Carotid artery was catheterized in 10 fetuses and descending aorta in 7fetuses. After a 4-day recovery, baseline measurements of fetal arterial blood pressures, blood gas values, and fetal cardiovascu-lar hemodynamics by pulsed Doppler ultrasonography were obtained under isoflurane anesthesia. Comparable data to baselinewere collected 10 min (acute hypoxemia) and 60 min (prolonged hypoxemia) after maternal hypo-oxygenation to saturation levelof 70%–80% was achieved. During prolonged hypoxemia, pH and base excess (BE) were lower and lactate levels were higher inthe descending aorta than in the carotid artery. During hypoxemia mean arterial blood pressure (MAP) in the descending aortaincreased, whereas in the carotid artery, MAP decreased. In addition, right pulmonary artery pulsatility index values increased,and the diastolic component in the aortic isthmus bloodflow velocity waveform became more retrograde, thus decreasing theaortic isthmus antegrade/retrograde bloodflow (AoI Net Flow) ratio. Both fetal ventricular cardiac outputs were maintained evenduring prolonged hypoxemia when significant fetal metabolic acidemia developed. Fetal chemoreflex activation induced by hy-poxemia decreased the perfusion pressure in the cerebral circulation. Fetal weight-indexed left ventricular cardiac output (LVCO)or AoI Net Flow ratio did not correlate with a drop in carotid artery blood pressure.