کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3007568 | 1181378 | 2006 | 11 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: The heart–brain interaction in the fetus: Cerebrovascular blood flow in the developing human The heart–brain interaction in the fetus: Cerebrovascular blood flow in the developing human](/preview/png/3007568.png)
Fetal blood flow is influenced by multiple factors, including the structure of the heart and the impedance of the distal vascular beds. Many babies with congenital heart disease have restricted intrauterine growth, neurologic abnormalities, and poor neurodevelopmental outcome, independent of surgical intervention. The circulatory alterations that accompany specific anatomic cardiac defects may lead to predictable blood flow disturbances that affect normal brain development.Doppler measurements of vascular resistance in the cerebral circulation and calculations of resistance ratios that quantitate fetal blood flow distribution are altered in growth retarded fetuses and are predictive of growth retardation and poor perinatal outcome in high risk pregnancies. Fetuses with normal hearts but compromised placental perfusion have a compensatory redistribution of blood flow that is believed to enhance cerebral perfusion. This phenomenon, termed “brain sparing”, is due to a decrease in cerebral vascular resistance, which is likely initiated and controlled by an autoregulatory mechanism. Failure of this mechanism to adequately compensate for cerebral hypoxemia in fetuses with congenital heart disease may result in the disproportionate intrauterine growth and neurodevelopmental abnormalities that occur in many of these infants. Investigators have only begun to study whether “brain sparing” occurs in fetuses with congenital heart disease and to determine if alterations in cerebral perfusion impact on fetal neurodevelopment and postnatal neurologic outcome for these high-risk infants.
Journal: Progress in Pediatric Cardiology - Volume 22, Issue 1, May 2006, Pages 41–51