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Showing papers on "Fetus published in 1979"


Journal ArticleDOI
TL;DR: Pulmonary arterial pressures and flows in utero and changes during gestation; patterns of fetal pulmonary blood flow; factors that influence fetal pulmonary vascular responses; and mechanisms responsible for the postnatal decrease in pulmonary vascular resistance are considered.
Abstract: During fetal life, gas exchange is carried out in the placenta. The lung does not have a physiological role, apart from possible metabolic functions which include secretion of hormones, enzymatic conversion of inactive substances to functional hormones, and degradation of active materials to inactive metabolites. Blood flow through the lungs is quite low during fetal life; most of the systemic and umbilical venous blood returning to the heart is shunted through the foramen ovale to the left atrium and left ventricle, or through the ductus arteriosus directly from the pulmonary trunk to the descending aorta. About 85-90% of the blood ejected by the right ventricle is diverted from the lungs through the ductus arteriosus (48). Because the right ventri­ cle ejects about 66% of the combined ventricular output of the fetal heart, about 60% of the total output of the heart passes through the ductus arteriosus and thus does not enter the lungs. Should this volume of blood pass through the pulmonary circulation and return to the left ventricle, there would be an unnecessary increase in the volume of work placed on the heart. The low fetal pulmonary blood flow has been explained on the basis of a high pulmonary vascular resistance. Mter birth, however, a marked in­ crease in pulmonary blood flow is necessary to permit adequate gas ex­ change. This review considers: (0) pulmonary arterial pressures and flows in utero and changes during gestation; (b) patterns of fetal pulmonary blood flow; (c) factors that influence fetal pulmonary vascular responses; and (d) mechanisms responsible for the postnatal decrease in pulmonary vascular resistance.

334 citations


Journal ArticleDOI
TL;DR: Children born to mothers who smoke are more likely to suffer from respiratory problems such as asthma, problems of the ear, nose and throat and may have a physical or learning disability.
Abstract: Smoking during pregnancy can lead to a higher risk of miscarriage, complications during labour, low birth weight and sudden infant death. Smoking during pregnancy increases the risk of infant mortality by an estimated 40%. Children born to mothers who smoke are more likely to suffer from respiratory problems such as asthma, problems of the ear, nose and throat and may have a physical or learning disability. (Public Health England).

221 citations


Journal ArticleDOI
TL;DR: Data showed that the fetal glucose pool was in equilibrium with the maternal glucose pool in both normal and diabetic subjects, indicating that a brief maternal fast did not initiate systemic glucose production in human fetus.
Abstract: The effects of pregnancy and diabetes on systemic glucose production rates and the sources of glucose for the human fetus in utero were evaluated in five normal, four gestationally diabetic, and one insulin-dependent diabetic subject undergoing elective caesarean section at term gestation. Five normal nonpregnant women were studied for comparison. Systemic glucose production rates were measured with stable tracer [1-(13)C]glucose according to the prime-constant rate infusion technique. Even though the plasma glucose concentration during normal pregnancy had declined as compared with the nonpregnant subjects (P < 0.0005), the systemic glucose production rate was 16% greater, a rate sufficient to provide the glucose requirement of the fetus at term gestation. The decline in glucose concentration could be the result of an increase in apparent volume of distribution of glucose. Systemic glucose production rates in well-controlled, gestationally diabetic subjects were similar to those in normal pregnant subjects (2.07+/-0.53 vs. 2.42+/-0.51 mg/kg.min). The sources of glucose for the human fetus at term gestation were evaluated by comparing (a) natural variation in (13)C:(12)C ratio of plasma glucose and (b) enriched (13)C:(12)C ratio of plasma glucose during [1-(13)C]glucose infusion in maternal and fetal blood at delivery in both normal and diabetic subjects. These data showed that the fetal glucose pool was in equilibrium with the maternal glucose pool in both normal and diabetic subjects, indicating that a brief maternal fast did not initiate systemic glucose production in human fetus. A materno-fetal gradient was observed for betahydroxybutyrate.

210 citations


Journal ArticleDOI
01 Dec 1979-Diabetes
TL;DR: Based on the similar DNA concentrations and protein/DNA ratios observed in hyperinsulinemic and control groups, the hepatomegaly appears to be the result of insulin-stimulated hyperplasia and not of hypertrophy.
Abstract: The delivery of 19 U of insulin a day for 21 days to the rhesus monkey fetus, coupled with the permeability properties of the placenta, has made it possible to produce fetal hyperinsulinemia in the presence of euglycemia. Fetal plasma insulin concentrations of 3525 μU/ml were attained with no apparent effects on the mother. In fetal macrosomia, a 34% increase in body weight was observed above the expected weight for gestational age (466 vs. 348 g). Relative organomegaly, matched for gestational age of fetal weight, was seen in the hyperinsulinemic fetuses with enlarged livers, placentas, hearts, and spleens. Liver composition in the fetuses was only slightly affected by hyperinsulinemia. Glycogen concentration was elevated, but not sufficiently, to explain the relative hepatomegaly produced. The lipid, protein, DNA, and RNA concentrations were not affected by hyperinsulinemia. Based on the similar DNA concentrations and protein/DNA ratios observed in hyperinsulinemic and control groups, the hepatomegaly appears to be the result of insulin-stimulated hyperplasia and not of hypertrophy. In the presence of normal plasma concentrations of growth substrates, insulin in the subhuman fetus has been shown to be a growth-promoting hormone that has specific growth-stimulating effects.

201 citations


BookDOI
01 Jan 1979
TL;DR: This 6th Edition maintains it's pre-eminence as the major repository of facts about prenatal diagnosis as a critical analysis and synthesis of established and new knowledge based on the long experience of authorities in their respective fields.
Abstract: Genetic disorders and the fetus , Genetic disorders and the fetus , کتابخانه مرکزی دانشگاه علوم پزشکی تهران

172 citations


Journal ArticleDOI
TL;DR: The results indicate that preservation of an upper motor neurone supply to the phrenic nucleus is of critical importance for fetal lung growth, and confirm the growth-promoting effects of liquid distension of the fetal lungs.

167 citations


Journal ArticleDOI
TL;DR: Pure populations of large, nucleated erythrocytes derived from yolk sac blood islands were obtained during normal fetal mouse development and Embryonic hemoglobins were present in these cells early in gestation, as demonstrated by both biochemical and immunocytochemical techniques.
Abstract: Pure populations of large, nucleated erythrocytes derived from yolk sac blood islands were obtained during normal fetal mouse development. Embryonic hemoglobins were present in these cells early in gestation. Later in gestation, an increasing amount of adults hemoglobin was also synthesized and accumulated in this population of primitive nucleated erythrocytes, as demonstrated by both biochemical and immunocytochemical techniques.

165 citations


Journal ArticleDOI
TL;DR: This case study suggests that bromocriptine crosses the human placenta and affects the fetal pituitary, maternal GH does not influence fetal or amniotic GH, and amniotics fluid PRL correlates poorly with either maternal or fetal blood levels and is not affected by bromOCriptine.
Abstract: An unexpected 20-week-old pregnancy was found in a young acromegalic who had been treated with 10 mg bromocriptine/day for 10 months. The drug was continued throughout the period of gestation. No growth of the pituitary adenoma was noticed. The intrauterine development of the fetus was normal. Bromocriptine therapy had no discernible effect on the expected patterns of secretion of placental hormones, but inhibited completely the increase of PRL in the serum of the mother. Maternal plasma GH concentrations were very high in spite of the treatment and progressively declined after delivery. The plasma GH level was normal in the child, but PRL was very low at birth and increased in the following days. The expected high PRL concentration was found in the amniotic fluid. This case study suggests that bromocriptine crosses the human placenta and affects the fetal pituitary, maternal GH does not influence fetal or amniotic GH, and amniotic fluid PRL correlates poorly with either maternal or fetal blood levels and...

137 citations



Journal ArticleDOI
TL;DR: Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus, fetal pulmonary arterial hypertension, and right ventricular damage, and this mechanism may be one cause of persistent pulmonary hypertension due to vasoconstriction and increased pulmonary arteria smooth muscle and/or tricuspid insufficiency.
Abstract: The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in a significant rise in the fetal pulmonary-to-systemic arterial mean blood pressure difference across the ductus arteriosus, presumably secondary to constriction of the ductus arteriosus. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of prostaglandin E1 (PGE1) into the fetal inferior vena cava. Fetal lungs from study and control animals were fixed by perfusion at measured pulmonary arterial mean blood pressure, and fifth-generation resistance vessels were studied. The medial width/external diameter ratio was significantly increased in the study vs the control lungs due to increased smooth muscle and decreased external diameter. In addition, study fetuses had acute degenerative myocardial changes in the tricuspid valve papillary muscles, the right ventricular free wall and the interventricular septum. Similar changes were not seen in control fetuses. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus, fetal pulmonary arterial hypertension, and right ventricular damage. If severe, this may cause rapid fetal death. If less severe, in the newborn infant, this mechanism may be one cause of persistent pulmonary hypertension due to vasoconstriction and increased pulmonary arterial smooth muscle and/or tricuspid insufficiency due to papillary muscle infarction.

123 citations


Journal ArticleDOI
TL;DR: HLA typing indicated that the fetus would be an unaffected, phenotypically normal carrier of the disease gene, and this prediction was confirmed after birth.

Journal ArticleDOI
TL;DR: In this article, maternal and cord blood determinations of the ions and hormones involved in calcium homeostasis were made in pre-eclamptic women treated with intravenous magnesium sulfate.

Journal ArticleDOI
03 Aug 1979-Science
TL;DR: Thyroid function returned to normal from age 18 through 60 days in spite of continued iodide administration, strongly suggesting that resistance to the inhibitory effect of iodide on thyroid hormone synthesis is developed at approximately 18 days of age.
Abstract: The administration of iodide to pregnant and nursing rats induces hypothyroidism in the term fetus and neonatal rat through age 10 days as indicated by an increase in the serum concentration of thyroid-stimulating hormone and a decrease in the serum of thyroxine and triiodothyronine. Thyroid function returned to normal from age 18 through 60 days in spite of continued iodide administration, strongly suggesting that resistance to the inhibitory effect of iodide on thyroid hormone synthesis is developed at approximately 18 days of age. This perinatal rat model can be used to study the mechanisms responsible for iodide-induced hypothyroidism and goiter in human newborns whose mothers received iodide-containing medications during pregnancy.

Book ChapterDOI
01 Jan 1979

Journal ArticleDOI
TL;DR: It is suggested that cigarette smoking during pregnancy induces fetal hypoxia through two independent but additive pathways: (1) An acute effect is caused by nicotine activation of adrenergic discharge, resulting in vasoconstriction, a decreased uterine perfusion, and a consequent transient fetal tachycardia and (2) a delayed but prolonged increase in HbCO may cause a sustained reduction of fetal oxygenation.

Journal ArticleDOI
TL;DR: The effects of chronic alcohol administration and acute maternal oral alcohol intake on fetal development in rats were investigated and decrease in body, brain, heart, kidney, and liver weight did not appear to be due to zinc deficiency.
Abstract: The effects of chronic alcohol administration and acute maternal oral alcohol intake on fetal development in rats were investigated, both regimens causing substantial increase in fetal mortality. Decreased body, brain, heart, kidney, and liver weight did not appear to be due to zinc deficiency.

Journal ArticleDOI
TL;DR: There was a sex difference in the levels of all the androgenic steroids in the amniotic fluid before 20 weeks with higher levels in pregnancies with male fetuses and there was no correlation between the steroid levels in the maternal serum and amniotics fluid.

Journal Article
TL;DR: In this paper, the authors concluded that gestational diabetes is an acquired condition in pregnant rats, which is not perceptible in basal conditions, but become apparent in situations stressing the beta-cell activity, such as an intravenous glucose load or pregnancy.
Abstract: Intrvenous injection of 30 mg of streptozotocin per kg body weight induces a mild diabetes in pregnant rats (first generation); the non-fasting blood glucose is increased and the percentage of endocrine tissue and also the percentage of granulated beta cells do not increase. The fetuses of these mildly diabetic pregnant rats have an increased percentage of pancreatic endocrine tissue and there is beta-cell degranulation. The modifications in the endocrine pancreas during intrauterine life causes persistent changes in later adult life (second generation), which are not perceptible in basal conditions, but become apparent in situations stressing the beta-cell activity, such as an intravenous glucose load or pregnancy. During pregnancy in the second generation rats an increased non-fasting blood glucose and no adaptation of the beta cells is seen. This inadequate adaptation to pregnancy causes changes in the fetal endocrine pancreas of the fetuses of the third generation. From these experiments it may be concluded that gestational diabetes is an acquired condition.

Journal ArticleDOI
TL;DR: Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus and fetal pulmonary arterial hypertension which, if severe, may cause rapid fetal death, and it is possible that this mechanism may be one cause of persistent pulmonary hypertension or tricuspid insufficiency or both in the newborn infant.

Journal ArticleDOI
TL;DR: Results verify accelerated lung maturation in certain complicated pregnancies, and no newborn infant developed respiratory distress syndrome in the presence of PG.

Journal ArticleDOI
TL;DR: The data suggest that the concept of the feto-placental unit would not apply to the cow and that restrictions concerning other generalized theories have to be applied.

Journal ArticleDOI
TL;DR: Changes in fetal and maternal plasma cortisol, progesterone, estrone, estradiol, and PRL were determined in response to infusion of dexamethasone into mothers and ACTH, TRH, PRL, hCG, or α-MSH into fetuses.
Abstract: In utero regulation of primate fetal adrenal glands and their role in steroidogenesis were studied between days 125-143 of gestation (term, 167 days) in chronically catheterized rhesus monkeys. Changes in fetal and maternal plasma cortisol, progesterone, estrone, estradiol, and PRL were determined in response to infusion of dexamethasone into mothers and ACTH, TRH, PRL, hCG, or α-MSH into fetuses. Significant, (P 0.05). Despite continued supp...

Book ChapterDOI
01 Jan 1979
TL;DR: At the Nutricia Symposium in Groningen in 1973 Professor Visser et al. gave a paper on “Parenteral nutrition in low birth weight infants” (I).
Abstract: At the Nutricia Symposium in Groningen in 1973 Professor Visser et al. gave a paper on “Parenteral nutrition in low birth weight infants” (I). In the discussion afterwards the question was raised as to whether the low birth weight infant should receive an amino acid mixture corresponding to human milk, or to fetal plasma, and it was suggested that the best mixture might be one corresponding to that of the baby’s body itself. At that time there were no figures for the amino acid make-up of the protein in the body of the human fetus. I promised that such information would be forthcoming, and this is the main subject of our paper today.

Journal Article
TL;DR: Under normal conditions of placental perfusion, glucose transfer is approximately 15% less than it would be if placental blood flows were infinitely large.
Abstract: The rates of glucose transfer from maternal blood to pregnant uterus and from placenta to fetus were measured in eight sheep at spontaneously occurring glucose concentrations (control state) and while the fetus, the mother, or both were receiving a constant infusion of glucose. In addition two fetuses received insulin infusions. In the control state the net glucose flux from placenta to fetus was only 27 +/- 2.6% (SEM) of the net flux from the uterine circulation to the pregnant uterus. An empirical equation describing the relationship between placental glucose transfer and arterial plasma glucose concentrations was derived from the data and compared with equations constructed on the basis of methematical models of placental function. This analysis indicates that: (1) placental glucose transfer is mediated by carriers with Km approximately equal to 70 mg/dl; (2) the rate of glucose transfer from mother to fetus is limited primarily by the transport characteristics and glucose consumption rate of the placenta; (3) under normal conditions of placental perfusion, glucose transfer is approximately 15% less than it would be if placental blood flows were infinitely large.

Journal ArticleDOI
TL;DR: In rats, of the Wistar-Porton strain, a single intravenous injection of 1.25 mg Cd2+ between days 9 and 15 of gestation results in a high incidence of hydrocephalus, together with other malformations in the fetuses, examined on day 20.
Abstract: In rats, of the Wistar-Porton strain, a single intravenous injection of 1.25 mg Cd2+ between days 9 and 15 of gestation results in a high incidence (80% of hydrocephalus, together with other malfor...

Journal ArticleDOI
TL;DR: The most significant fetal pulmonary changes observed were increases in maximum lung volumes, and the fact that comparable increases in peak volumes were demonstrated on saline filling supports contention that these changes are related primarily to lung structural alterations rather than surfactant effects.

Journal ArticleDOI
TL;DR: The importance of insulin in fetal development is illustrated by the following case presentation, a severely growth-retarded infant who possessed no detectable pancreatic tissue at postmortem examination.
Abstract: Recent investigations support the concept that insulin is a primary growth hormone during fetal life. The importance of insulin in fetal development is illustrated by the following case presentation, a severely growth-retarded infant who possessed no detectable pancreatic tissue at postmortem examination. CASE REPORT Patient B.G.C. was born following an uncomplicated pregnancy to a 19-year-old gravida 1, para 0, abortus 1 mother by emergency Cesarean section for fetal distress. The baby weighed 1,350 gm with Apgar scores of 2 at one minute, 2 at five minutes, and 4 at ten minutes, requiring immediate intubation and ventilation. Gestational age was 41 weeks by dates, 36 to 37 weeks by clinical examination, and greater than 36 weeks by radiologic evidence of teeth calcification.1

Journal ArticleDOI
TL;DR: It is suggested that target antigens for maternal lymphocytes are present on the placenta, a structure critical to the continuance of pregnancy, and that the presence of the blocking antibody is necessary for fetal well‐being.


Journal ArticleDOI
TL;DR: The presence of this enzyme may allow the fetus liver to remove circulating triglycerides and to store them in preparation for early extrauterine life.