Cerebral circulatory responses of near-term ovine fetuses during sustained fetal placental embolization.

To test the hypothesis that, in response to an increase in placental vascular resistance and progressive fetal asphyxia, the changes in external carotid blood flow waveforms are directly related to changes in external carotid vascular resistance, we embolized the fetal side of the placenta in pregnant sheep and measured cerebral and external carotid artery circulatory changes in relation to changes in external carotid artery flow waveforms. Chronically catheterized fetal sheep at 0.85 of gestation were embolized ( n = 11) in the descending aorta for 6 h, until fetal arterial pH fell to ∼6.90. Fetuses became rapidly hypoxemic ( P < 0.0001) and developed a mixed respiratory and metabolic acidosis ( P< 0.0001 for [Formula: see text], pH, and base excess). There was a transient 40% increase in external carotid blood flow at pH ∼7.25 and a parallel 32% increase in fetal arterial blood pressure (both P < 0.01), whereas the external vascular resistance remained unaltered. Cerebral blood flow increased by 130% ( P < 0.0001), and cerebral vascular resistance decreased by 125% ( P < 0.0001) throughout the study. The external carotid resistance index (RI) decreased by 32% ( P < 0.0001) at the time external carotid vascular resistance remained unchanged. This fall in external carotid RI was due almost entirely to a 110% increase in external carotid fundamental impedance ( P < 0.001). We conclude that the poor relationship between the changes in external carotid vascular resistance and RI indicated that other hemodynamic factors such as vascular impedance to pulsatile flow must be measured for correct interpretation of changes in flow waveform shape under hypoxic conditions. In addition, changes in external carotid blood flow were not proportional to changes in cerebral blood flow in this model.