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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fetal hypoxia secondary to uterine vascular insufficiency was induced by injecting norepinephrine or PGE2 into the maternal circulation of near-term sheep. With these drugs the uterine blood flow fell to 41 and 40% of its control value, respectively. The fetal responses to the PGE2-induced uterine contraction were a bradycardia which was apparent within 10 seconds (P less than 0.05), and a hypertension which was also apparent within 10 seconds (P less than 0.03). After the norepinephrine-induced uterine vasoconstriction, there was no observable change in the fetal arterial pressure. The fetal heart rate started to fall after 30 to 60 seconds and started to return to the control value within 90 seconds. The fetal response to uterine vascular insufficiency induced by a contraction may not have been caused by hypoxia alone as these responses were more rapid in onset than the fetal responses observed subsequent to uterine vascular insufficiency produced by vasoconstriction.
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PMID:The effect of uterine vascular insufficiency on fetal arterial pressure and heart rate in the near-term sheep. 89 99

122 cases of high risk pregnancies, consisting of mainly pregnancy-induced hypertension (PIH), medical complications, postmaturity and suspected distress were periodically monitored with 11 biophysical and biochemical assays. Positive prediction accuracy rate was analyzed with a neonatal UA pH less than 7.20 as the criterion of fetal hypoxia and ischemia. A number of predicting items together, namely: NST, the other Manning's 4 items, internal monitoring with abnormal Cardiotocography, meconium deeply stained amniotic fluid, FBS pH less than 7.2, uterine contraction time lasting greater than 37 sec and interval shorter than 70 sec, gave the best sensitivity, specificity, positive and negative prediction rates and total accuracy rate of 71.69%, 84.06%, 77.55%, 79.45% and 78.68% respectively. The causes for false positive and false negative cases were discussed. Special attention must be paid to those cases with low UA pH al though normal Apgar scores during the neonatal period.
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PMID:[Early diagnosis of fetal distress and neonatal asphyxia]. 191 52

The intrauterine fetal status was assessed in women at 34-42 week gestation; the pregnancies were complicated by obstetric and extragenital disease (nephropathy, prolonged gestation, hypertension, diabetes mellitus, renal disease). Computer-assisted analysis of the diagnostic value of fetal cardiotocography, uterine-placental hemodynamics, and acid-base status of maternal capillary blood showed that the following parameters are most informative for the diagnosis of chronic fetal hypoxia: stable rhythm duration; oscillation amplitude; acceleration/deceleration number, amplitude, and duration; volume flow rate of the uterine-placental unit; and pH and base deficiency in the blood taken from the cervix uteri.
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PMID:[Diagnosis of chronic fetal anoxia]. 222 50

Doppler blood flow velocity waveforms from fetal umbilical artery, descending aorta, internal carotid artery and maternal uterine arteries were recorded in 50 fetuses near term undergoing cesarean section before the onset of labor in order to evidence eventual relationships with the fetal acid-base status. The primary indications for cesarean section were in 16 cases an elective repeated cesarean section and in the remaining cases maternal hypertension often associated with fetal growth retardation and/or fetal distress. The technique of anesthesia was strictly standardized and fetal blood gas levels and acid-base status were analyzed in umbilical artery and vein immediately after birth. A significant correlation was found between the pulsatility index from internal carotid artery and the pO2 levels in umbilical vein (r = 0.87; p less than or equal to 0.001). Similar relationships were found between the pulsatility index from descending aorta and the pCO2 (r = 0.78; p less than or equal to 0.001), base excess (r = 0.72; p less than or equal to 0.001) and pH (r = 0.80; p less than or equal to 0.001) levels in umbilical artery. It is suggested that Doppler ultrasound could be useful in the diagnosis of fetal hypoxia and acidosis.
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PMID:Are blood flow velocity waveforms related to umbilical cord acid-base status in the human fetus? 274 20

We undertook analyses to determine if fetal, intrapartum, and neonatal hypoxia are important causes of low IQ values. We analyzed prospectively collected pregnancy, perinatal, and subsequent developmental data for 19,117 children. As expected, sociohereditary and demographic factors had a large influence on IQ scores. Taking these latter influences into consideration, nothing that happened during labor, delivery, or the neonatal period affected subsequent IQ values. The same was true for early pregnancy disorders that can produce acute fetal hypoxia. By contrast, antenatal disorders and conditions that can produce subacute or chronic fetal hypoxia correlated with low IQ values. These antenatal disorders and conditions were maternal gestational anemia, relative gestational hypotension, hypertension, multiple births, and fetal growth retardation. All of these findings were the same whether neurologic abnormalities were absent or present, suggesting that the same factors were sometimes involved in the genesis of cognitive impairments and neurologic abnormalities.
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PMID:Antenatal hypoxia and low IQ values. 378 82

Gated, pulsed, doppler ultrasound was used to study blood flow velocity profiles in the uterine vessels (arcuate arteries) during the second and third trimesters of pregnancy. A frequency index profile nomogram was constructed from 30 normal pregnancies; this demonstrated high diastolic velocity and low pulsatility. Among 31 pregnancies with complications 14 showed waveform changes suggesting raised vascular resistance; these pregnancies were complicated with a high frequency of proteinuric hypertension, poor fetal growth, and fetal hypoxia. This non-invasive technique may give early warning of impaired uteroplacental perfusion and can be used to evaluate methods of improving uterine blood flow.
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PMID:New doppler technique for assessing uteroplacental blood flow. 613 39

Pheochromocytoma accounts for only 0.1% of hypertension found in adults between 40 and 70 years of age. Although it is extremely rare in pregnancy, if it occurs and is unrecognized in pregnant women, pheochromocytoma can have catastrophic effects. For instance, maternal fatal hypertension can be precipitated by anesthesia, vaginal delivery, uterine contractions, or even vigorous fetal movements. Fetal growth retardation is often seen secondary to decreases in uteroplacental perfusion. Fetal hypoxia or death can also occur with maternal episodes of headache, palpitations, and diaphoresis related to tumor secretions. Because many of the signs and symptoms of pheochromocytoma are similar to more frequently encountered hypertensive syndromes related to pregnancy, the diagnosis of pheochromocytoma can be easily overlooked. The case report presented here illustrates the difficulties associated with the diagnosis of pheochromocytoma in a pregnant patient, highlights problems encountered by patients with the tumor, and reviews diagnostic and treatment approaches.
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PMID:Pheochromocytoma in a pregnant patient. 812 12

1. In seven unanaesthetized fetal sheep (> 80% term), isocapnic hypoxia (arterial partial pressure of O2, Pa,O2, approximately 15 mmHg) was induced for 1 h by lowering maternal inspired PO2. Fetal hypoxia was also produced during intra-arterial administration of the adenosine receptor antagonist 8-(p-sulphophenyl)-theophylline (8-SPT). The fetal 8-SPT infusion was begun just prior to hypoxia and was stopped when fetal Pa,O2 was returned to normal. 2. Hypoxia induced a progressive fetal acidosis, a rise in mean arterial pressure, a transient fall in heart rate and a decrease in breathing movements. 8-SPT significantly reduced the metabolic acidosis and abolished the hypertension and bradycardia without altering hypoxic inhibition of fetal breathing. Administration of the vehicle for 8-SPT during hypoxia did not significantly affect the normal fetal metabolic and cardiovascular responses to acute O2 deprivation. 3. It is concluded that adenosine mediates the fetal bradycardia and hypertension produced by hypoxia, indicating that adenosine modulates fetal autonomic responses to acute oxygen deficiency. Secondly, adenosine contributes to fetal metabolic acidaemia, suggesting that adenosine also modulates fetal glycolytic responses to hypoxia.
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PMID:Adenosine mediates metabolic and cardiovascular responses to hypoxia in fetal sheep. 857 65

The early-onset type (onset earlier than 28 gestational weeks) of pregnancy induced hypertension (PIH) has the clinical characteristics of a high incidence of intrauterine growth retardations (IUGR), fetal distress, neonatal hypoglycemia and hypertensive disposition. Moreover, the infants from early-onset type of PIH mothers showed a statistically significant higher incidence of neurological handicap (cerebral palsy, mental retardation and epilepsy) than late onset type. The infants with a neurological handicap had severe IUGR and intractable hypoglycemia in the early neonatal period, probably due to low storage of glucose in the liver and fetal hypoxia. Appropriate perinatal management, including proper evaluation of fetal well-being and good timing of delivery, could improve the outcome of infants from early-onset type of PIH mothers.
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PMID:Neonatal hypoglycemia in infants with intrauterine growth retardation due to pregnancy-induced hypertension. 920 Aug 79

The purpose of this study was to estimate if the erythropoietin (EPO) concentration in cord arterial blood can be an indicator of a fetal risk. We studied EPO concentration measured by enzyme immonoassay in ten patient groups: (1) control group with healthy newborns (n = 72); (2) neonates born by elective caesarean section (n = 16); (3) newborns with acidosis at birth (n = 12); (4) newborns with 1-min-Apgar < 7 (n = 8); (5) preterm neonates (n = 25); (6) newborns with gestational age > or = 242 weeks (n = 19); (7) neonates born to mothers with hypertension (n = 16); (8) newborns with signs of fetal distress in CTG (n = 29); (9) neonates born to mothers with diabetes (n = 19), divided into two subgroups: diabetes White A-D (n = 8) and gestational diabetes (n = 11); (10) neonates born to mothers with diabetes White A-D and with acidosis at birth (n = 7). The geometric mean was 26.4 mU/ml in the control group. EPO levels was found significantly increased (p < 0.01) in the following groups: (3) newborns with acidosis (52 mU/ml); (6) newborns with gestational age > or = 242 weeks (63.5 mU/ml); (8) newborns with signs of fetal distress in CTG (47.1 mU/ml); (9) neonates born to mothers with diabetes White A-D (47.7 mU/ml); (10) neonates born to mothers with diabetes White A-D and with acidosis at birth (> 64 mU/ml). We came to the conclusion that the cord arterial EPO concentration indicates a chronic fetal hypoxia and a longer duration of hypoxia before birth.
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PMID:[Erythropoietin as a marker of perinatal risk]. 971 26


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