The objective of the present study was to determine the characteristics of Doppler flow velocity wave forms in branch pulmonary arteries in relation to gestational age. A total of 111 singleton normal pregnancies were studied during the second half of pregnancy using a combined color-coded Doppler and two-dimensional real-time ultrasound system. Pulsed Doppler measurements of the most proximal branch of the right or left pulmonary artery were attempted during fetal apnea from a transverse cross-section of the fetal chest at the level of the cardiac four-chamber view after visualization with color Doppler. The success rate in obtaining the pulmonary arterial wave form was 85%. The wave form displayed a rapid systolic velocity acceleration, followed by an initially rapid but then more gradual velocity deceleration which was interrupted in most cases by a short reversed flow interval at the beginning of the diastolic phase of the cardiac cycle. The diastolic phase was characterized by forward flow. Peak systolic, end-diastolic and time-averaged velocity, pulsatility index, and systolic integral remained constant during gestation. Changes in vessel diameter or compliance may play a role in this. A gestational age-dependent rise was established for peak diastolic velocity, diastolic integral, and early peak diastolic reverse flow, whereas a gestational age-determined decline was found for the peak systolic/peak diastolic ratio. Fetal heart rate demonstrated a statistically significant increase relative to gestational age. However, the observed relation between the flow velocity wave form parameters, pulsatility index calculations, and gestational age was independent of fetal heart rate. It is speculated that peak diastolic velocity, diastolic integral, and peak systolic/peak diastolic ratio rather than the pulsatility index are useful in detecting gestational age-related changes in human fetal pulmonary vascular resistance.
There was a 17-fold rise in mean dorsal aortic blood flow (mm3/s). Heart rate doubled from 123 .C 12 to 239 f 8 bpm, and stroke volume increased from 0.14 f 0.08 to 1.28 2 0.55 mm3. A stage-related rise was seen in peak systolic and mean velocities and peak acceleration. These data may serve as a basis for flow velocity wave form investigation and interpretation in developmental stages of cardiac malformations. (Pediatr Res 34: 44-46, 1993) High-resolution real-time ultrasound and Doppler techniques allow detailed analysis of human fetal cardiac anatomy and function during the second half of pregnancy. A reliable diagnosis of a wide range of cardiac anomalies can now be made (1-3), and as a result, a spectrum of cardiac pathology has emerged that appears to be different from that seen in postnatal life (4). Moreover, Doppler studies have demonstrated abnormal flow velocity patterns in the outflow tract in the presence of atrioventricular and semilunar valve pathology (5).In the developing heart, morphogenesis and hemodynamic function are closely linked. Micro-Doppler and pressure studies in chick embryos have provided valuable information on this relationship in normal heart development (6, 7). T o study the interaction between hemodynamics and morphology in abnormal heart development, an animal model with specific and reproducible cardiac malformations is needed. We recently developed a standardized method for inducing a spectrum of double-outlet right ventricle in the stage 35 chick embryo (8). Moreover, for future studies on hemodynamics associated with abnormal heart development, normal data on flow velocity parameters from stage 20 up to stage 35 must be collected.In this article, we report on the validity, reproducibility, and normal values of dorsal aortic flow velocity wave forms in stage 20 to stage 35 chick embryos.
Our purpose was to study the nature and gestational age dependency of fetal venous Doppler flow velocity wave forms and their relationship with fetal arterial wave forms in early pregnancy. Venous and arterial Doppler recordings were performed in 262 normal singleton pregnancies according to a cross-sectional study design at 8-20 wk of gestation. A statistically significant age-dependent increase is established for the umbilical vein, ductus venosus, and inferior vena cava time-averaged velocity. Umbilical venous pulsatile flow patterns are observed up to 15 wk of gestation. The pulsatility index for veins in all three venous vessels displays a gestational age-dependent reduction. No relation can be established between the pulsatility index for veins and the pulsatility index in the descending aorta and umbilical artery. This may be explained by the fact that the pulsatility index for veins reflects cardiac ventricular preload, whereas the pulsatility index in the arterial vessels reflects downstream impedance at fetal placental level.
Arterial, venous, and intracardiac Doppler flow velocity waveforms were studied in 50 women with a small for gestational age (SGA) fetus according to a cross-sectional study design. No Doppler signals could be obtained in five women for technical reasons. The remaining 45 women were compared with normal control subjects matched for gestational age and maternal parity. The 45 SGA fetuses were divided into birth weight below the 5th centile for gestational age (group I, n = 35) and birth weight between the 5th and 10th centile for gestational age (group II, n = 10). A significant difference in baseline characteristics was found between both SGA subsets and normal controls. In SGA I fetuses, the pulsatility index in the umbilical artery and descending aorta was significantly higher, but lower in the middle cerebral artery when compared with normal controls. At the atrioventricular and venous level (umbilical vein, ductus venosus, and inferior vena cava) reduced time-averaged velocities were established. PIV in the ductus venosus and IVC showed a significant increase. Within the same SGA subset, no relationship could be established between arterial downstream impedance and 1) atrioventricular flow velocities and 2) pulsatility index in the ductus venosus and inferior vena cava. Also, no relationship existed between flow velocity waveforms and pregnancy-induced hypertension and admission to the neonatal intensive care unit. Umbilical venous pulsations and absent/reverse flow in the umbilical artery were associated with a high intrauterine mortality rate and low birth weights. In SGA II fetuses, the pulsatility index in the umbilical artery and descending aorta was significantly higher than in normal controls. It can be concluded that fetuses with a birth weight below the 5th centile demonstrate marked changes in arterial, atrioventricular, and venous flow velocity waveforms. Atrioventricular and venous flow velocity waveforms change independently from arterial downstream impedance, suggesting that other factors, such as reduced volume flow and myocardial contraction force, may play a role in the observed changes.
The course of plasma β-endorphin/β-lipotropin, cortisol and prolactin (PRL) levels was followed from 0.5 till 5 h after normal delivery in 13 healthy women. Six subjects who did not want to breast-feed their child received 2.5 mg bromocriptine orally 1 h after delivery. After 3 h the effect of the intravenous administration of 200 µg thyrotropin-releasing hormone (TRH) was also measured. Elevated plasma β-endorphin and cortisol levels decreased after delivery in a (log) linear fashion which was not influenced by bromocriptine. TRH elicited a significant short-lived identical increase in plasma β-endorphin/β-lipotropin concentrations in the control and the bromocriptine-treated subjects. TRH similarly delayed the rapid decline in plasma cortisol levels in both groups of women. Basal and TRH-induced PRL levels were rapidly suppressed by bromocriptine. These studies show the presence of a paradoxical increase of β-endorphin/β-lipotropin and cortisol levels in response to TRH occurring shortly after delivery in normal women. This response cannot be mediated by the placenta. The absence of an inhibiting effect of bromocriptine on basal and TRH-induced β-endorphin and cortisol release does not lend support to the hypothesis of the presence of a functionally active intermediate pituitary lobe in man early in puerperium.
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