The parturograph is a composite record designed for the monitoring of fetal and maternal well-being and the progress of labour. It permits the early recognition of abnormalities and pinpoints the patients who would benefit most from intervention. Observations are made from the time of admission of the mother to the caseroom and recorded graphically. Factors assessed include fetal heart rate, maternal vital signs and urine, cervical dilatation, descent of the presenting fetal part, and frequency, duration and intensity of uterine contractions. (+info)
Restriction of placental and fetal growth in sheep alters fetal blood pressure responses to angiotensin II and captopril.
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1. We have measured arterial blood pressure between 115 and 145 days gestation in normally grown fetal sheep (control group; n = 16) and in fetal sheep in which growth was restricted by experimental restriction of placental growth and development (PR group; n = 13). There was no significant difference in the mean gestational arterial blood pressure between the PR (42.7 +/- 2.6 mmHg) and control groups (37.7 +/- 2.3 mmHg). Mean arterial blood pressure and arterial PO2 were significantly correlated in control animals (r = 0.53, P < 0.05, n = 16), but not in the PR group. 2. There were no changes in mean arterial blood pressure in either the PR or control groups in response to captopril (7.5 microg captopril min-1; PR group n = 7, control group n = 6) between 115 and 125 days gestation. After 135 days gestation, there was a significant decrease (P < 0.05) in the fetal arterial blood pressure in the PR group but not in the control group during the captopril infusion (15 microg captopril min-1; PR group n = 7, control group n = 6). 3. There was a significant effect (F = 14.75; P < 0.001) of increasing doses of angiotensin II on fetal diastolic blood pressure in the PR and control groups. The effects of angiotensin II were different (F = 8.67; P < 0.05) in the PR and control groups at both gestational age ranges. 4. These data indicate that arterial blood pressure may be maintained by different mechanisms in growth restricted fetuses and normally grown counterparts and suggests a role for the fetal renin-angiotensin system in the maintenance of blood pressure in growth restricted fetuses. (+info)
Heart specific expression of mouse BMP-10 a novel member of the TGF-beta superfamily.
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Here we report the cloning and expression of murine BMP-10, a novel member of the TGF-beta superfamily. In the mouse embryo, BMP-10 expression begins at 9.0 d.p.c. and is restricted to the developing heart. Initially, BMP-10 expression localizes to the trabeculated part of the common ventricular chamber and to the bulbus cordis region. After 12.5 d.p.c., additional BMP-10 expression is seen in the atrial wall. The data presented here suggest that BMP-10 plays an important role in trabeculation of the embryonic heart. (+info)
YAC complementation shows a requirement for Wt1 in the development of epicardium, adrenal gland and throughout nephrogenesis.
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The Wilms' Tumour gene WT1 has important functions during development. Knock-out mice were shown to have defects in the urogenital system and to die at embryonic day E13.5, probably due to heart failure. Using a lacZ reporter gene inserted into a YAC construct, we demonstrate that WT1 is expressed in the early proepicardium, the epicardium and the subepicardial mesenchymal cells (SEMC). Lack of WT1 leads to severe defects in the epicardial layer and a concomitant absence of SEMCs, which explains the pericardial bleeding and subsequent embryonic death observed in Wt1 null embryos. We further show that a human-derived WT1 YAC construct is able to completely rescue heart defects, but only partially rescues defects in the urogenital system. Analysis of the observed hypoplastic kidneys demonstrate a continuous requirement for WT1 during nephrogenesis, in particular, in the formation of mature glomeruli. Finally, we show that the development of adrenal glands is also severely affected in partially rescued embryos. These data demonstrate a variety of new functions for WT1 and suggest a general requirement for this protein in the formation of organs derived from the intermediate mesoderm. (+info)
Cardiac blood flow studies in fetuses with homozygous alpha-thalassemia-1 at 12-13 weeks of gestation.
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OBJECTIVE: Fetuses affected by homozygous alpha-thalassemia-1 develop anemia as early as the first trimester. Our objective was to study hemodynamic indices in affected fetuses at 12-13 weeks of gestation to determine whether these would be useful in the prediction of anemia. DESIGN: Prospective observational study. SUBJECTS: Women referred before 14 weeks of gestation for the prenatal diagnosis of homozygous alpha-thalassemia-1. METHODS: Transabdominal and/or transvaginal Doppler sonography was performed to measure the flow velocities in the fetal ascending aorta and pulmonary artery at 12-13 weeks. The Doppler indices were compared between those that were subsequently confirmed to be affected by homozygous alpha-thalassemia-1 and those that were unaffected. RESULTS: Between June 1997 and April 1998, 60 eligible women were recruited. Doppler examination was successful in 58 fetuses. Of these, 22 were subsequently confirmed to be affected by homozygous alpha-thalassemia-1. The diagnosis was made by chorionic villus sampling and DNA analysis in two affected fetuses and by cordocentesis and hemoglobin evaluation in 20 affected fetuses. Hemoglobin concentrations could be measured in ten fetuses and these ranged from 4 to 8 g/dl. The affected fetuses had significantly higher peak velocities at the pulmonary valve and ascending aorta and a larger inner diameter of the pulmonary valve than that in unaffected fetuses. The total cardiac output was increased by one-third in affected fetuses and was mainly due to an increase of the right-side cardiac output. CONCLUSION: In the early stage of anemia, the fetus responds mainly by increasing its right-side cardiac output. However, there is extensive overlap of the values of cardiac output between the affected and the unaffected fetuses, precluding its use in the prediction of anemia. (+info)
Characteristics of blood flow in intrauterine growth-restricted fetuses with hypercoiled cord.
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OBJECTIVE: To clarify the characteristics of fetoplacental blood flow of growth-restricted fetuses with hypercoiled umbilical cord. SUBJECTS: Eight growth-restricted fetuses with hypercoiled cord. METHODS: Flow velocity waveforms of the umbilical cord artery and vein, fetal abdominal aorta and fetal inferior vena cava were analyzed. RESULTS: The resistance index in the umbilical artery in the hypercoiled cases was lower than that in normal fetuses. Early-diastolic reversed flow was observed in the abdominal aorta in some cases. In all cases, umbilical venous pulsation was observed in the entire cord until delivery. In one case, fetal heart failure occurred, resulting in pre-mature delivery. An atrophic type of single umbilical artery was observed in four cases. CONCLUSION: Fetal blood flow disturbance caused by a hypercoiled umbilical cord may be a cause of growth restriction. (+info)
Prevalence of aneuploidy with a cardiac intraventricular echogenic focus in an at-risk patient population.
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The objective of this study was to determine the relative risk for aneuploidy in the presence of a cardiac intraventricular echogenic focus in a patient population at high risk for aneuploidy. A retrospective cohort study was conducted on patients referred to a fetal diagnostic center who were undergoing amniocentesis. Records and second trimester sonograms were reviewed. Approximately 5100 comprehensive prenatal sonograms were obtained over a 2 year study period. Karyotyping by amniocentesis was done in 2412 women; 84 of the karyotypes (3.5%) were abnormal. Fetuses with no ultrasonographic findings suggestive of aneuploidy had a 1.4% (28 of 1940) prevalence of significant chromosomal abnormalities. An intraventricular echogenic focus was found in 149 of the women with karyotype analysis; 15 had an abnormal karyotype. Fetuses with intraventricular echogenic foci had a relative risk of 3.30 of aneuploidy when compared to fetuses without echogenic cardiac foci. The presence of an isolated intraventricular echogenic focus carried a relative risk of 4.08 compared to those fetuses in which ultrasonography had no finding associated with aneuploidy. In conclusion, these preliminary data indicate that presence of an intraventricular echogenic cardiac focus carries an increased risk of fetal aneuploidy. (+info)
Loss of a gp130 cardiac muscle cell survival pathway is a critical event in the onset of heart failure during biomechanical stress.
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Biomechanical stress is a major stimulus for cardiac hypertrophy and the transition to heart failure. By generating mice that harbor a ventricular restricted knockout of the gp130 cytokine receptor via Cre-IoxP-mediated recombination, we demonstrate a critical role for a gp130-dependent myocyte survival pathway in the transition to heart failure. Such conditional mutant mice have normal cardiac structure and function, but during aortic pressure overload, these mice display rapid onset of dilated cardiomyopathy and massive induction of myocyte apoptosis versus the control mice that exhibit compensatory hypertrophy. Thus, cardiac myocyte apoptosis is a critical point in the transition between compensatory cardiac hypertrophy and heart failure. gp130-dependent cytokines may represent a novel therapeutic strategy for preventing in vivo heart failure. (+info)