Xanthine oxidase and the fetal cardiovascular defence to hypoxia in late gestation ovine pregnancy.

Hypoxia is a common challenge to the fetus, promoting a physiological defence to redistribute blood flow towards the brain and away from peripheral circulations. During acute hypoxia, reactive oxygen species (ROS) interact with nitric oxide (NO) to provide an oxidant tone. This contributes to the mechanisms redistributing the fetal cardiac output, although the source of ROS is unknown. Here, we investigated whether ROS derived from xanthine oxidase (XO) contribute to the fetal peripheral vasoconstrictor response to hypoxia via interaction with NO-dependent mechanisms. Pregnant ewes and their fetuses were surgically prepared for long-term recording at 118 days of gestation (term approximately 145 days). After 5 days of recovery, mothers were infused i.v. for 30 min with either vehicle (n = 11), low dose (30 mg kg(-1), n = 5) or high dose (150 mg kg(-1), n = 9) allopurinol, or high dose allopurinol with fetal NO blockade (n = 6). Following allopurinol treatment, fetal hypoxia was induced by reducing maternal inspired O2 such that fetal basal P aO 2 decreased approximately by 50% for 30 min. Allopurinol inhibited the increase in fetal plasma uric acid and suppressed the fetal femoral vasoconstrictor, glycaemic and lactate acidaemic responses during hypoxia (all P < 0.05), effects that were restored to control levels with fetal NO blockade. The data provide evidence for the activation of fetal XO in vivo during hypoxia and for XO-derived ROS in contributing to the fetal peripheral vasoconstriction, part of the fetal defence to hypoxia. The data are of significance to the understanding of the physiological control of the fetal cardiovascular system during hypoxic stress. The findings are also of clinical relevance in the context of obstetric trials in which allopurinol is being administered to pregnant women when the fetus shows signs of hypoxic distress.

Environmental origins of congenital heart disease: the heart-placenta connection.

Although the mammalian embryo is well protected in the uterus, environmental chemicals, drugs, and maternal nutritional imbalances can interfere with regulatory pathways directing placental and embryonic development early in gestation. Embryonic cells are most susceptible to environmental influences during cellular specification and differentiation stages. Because biochemical differentiation precedes morphological outcome often by days, the period of susceptibility to environmental chemicals expectedly precedes visible morphogenic effects. The cellular mechanisms by which drugs and other environmental factors disrupt embryonic development and induce cardiac abnormalities have remained undefined.

Valor de los parámetros clínicos en el diagnóstico de una infección amniótica en gestantes con amenaza de parto prematuro / Value of clinical signs in the diagnosis of amniotic infection in patients with preterm labor

Objetivo: Estudiar el valor de la leucocitosis, fiebre materna y la taquicardia fetal en el diagnóstico de una infección amniótica.Sujetos y métodos: Un total de 113 gestantes con amenaza de parto prematuro a las que se les practicaron una amniocentesis y un cultivo de líquido amniótico. Al ingreso se tomó la temperatura axilar, se realizó un hemograma y se realizó un registro cardiotocográfico. Se relacionó la presencia de un cultivo de líquido amniótico positivo con la fiebre ( 37,8 °C), la taquicardia fetal ( 160 lat/min) y la leucocitosis materna (> 15.000 leucocitos/ml).Resultados: Trece de las gestantes (11,5 por ciento) presentaron una infección amniótica; 26 mujeres (23 por ciento) tuvieron una leucocitosis, cinco de ellas tenían un cultivo de líquido amniótico positivo (p = 0,1); 5 gestantes tuvieron fiebre, dos de ellas con un cultivo de líquido amniótico positivo (p = 0,1); 26 gestantes presentaron una taquicardia fetal (23 por ciento), ocho de las cuales tuvieron un cultivo de líquido amniótico positivo (p = 0,001). La sensibilidad de la taquicardia fetal para detectar una infección amniótica fue del 61,5 por ciento y la especificidad del 82 por ciento.Conclusión: La taquicardia fetal fue el único parámetro clínico que se asoció significativamente a la infección amniótica, aunque su valor predictivo positivo fue bajo. (AU)

Neonatal atrial flutter following fetal exposure to vibroacoustic stimulation.

The use of vibroacoustic stimulation (VAS) has become a common modality for testing fetal well being. A case of neonatal atrial flutter, following fetal exposure to VAS is presented. It should be emphasized that although VAS is a common and reliable test for evaluating fetal status, complications may occur.

[Vibration and acoustic stimulation during labor with external monitoring. Pathology of fetal heart rate]. / Estimulación vibroacústica en el trabajo de parto con monitorización externa. Patología de la frecuencia cardíaca fetal.

Vibratory acoustic stimulation was done in patients with an abnormal fetal heart rate tracing in external continuous electronic monitoring during labor, correlating with Apgar score, meconium staining and umbilical cord pH, describing a 83.3% sensitivity, 81.3% specificity and 62.5% positive predictive value. The authors recommend the use of vibratory acoustic stimulation in those cases with an abnormal fetal heart rate tracing in external continuous electronic monitoring, when we can not install internal electronic monitoring or obtain a fetal blood pH on assessment of fetal well-being.

The effect of maternal, labor, and fetal factors upon fetal heart rate during the intrapartum period.

The effect of maternal labor, and fetal characteristics upon fetal heart rate behavior during the intrapartum period has been studied in 400 patients. Abnormal labor in comparison to normal labor has a higher baseline fetal heart rate with an increased incidence of baseline tachycardia and an increased incidence of absent or decreased baseline variability. A decreasing fetal weight gestational age percentile is associated with an increased incidence of variable decelerations. Segmental epidural and Demerol analgesia carefully administered has little effect upon fetal heart rate behavior.

Human fetal oxygenation following paracervical block.

To test the hypothesis that fetal heart rate (FHR) changes following paracervical block may be secondary to fetal hypoxia, human fetal oxygenation was measured continuously using a transcutaneous electrode. Following the block, each fetus demonstrated a decline in oxygen tension (tcPO2) at 5 minutes, which reached its lowest value at a mean of 11.5 minutes and remained at this level for an average of 3 minutes. Following the block, FHR variability increased at 5.2 minutes. reaching its maximal level by a mean of 7.5 minutes. By 11 minutes, a decrease in FHR variability was noted, which lasted for approximately 17 minutes. Decreased variability was not uniformly associated with low tcPO2. On some occasions, fetal tcPO2 declined even in the absence of increased uterine activity, which was noted at times following the block. The severity of the tcPO2 decline appears related to the analgesic effectiveness of the block.

Post--paracervical block bradycardia: its prediction and preventability.

The fetal heart rate recordings of 100 parturients given PCB with less than 200 mg. of lidocaine were reviewed. No PCB bradycardia occurred if there were no pre-PCB FHR decelerations (92 per cent accuracy). In an effort to prevent post-PCB bradycardia, atropine was given in the maternal paracervical area and also intravenously. The most effective dose was 1.0 mg. intravenously, but the prophylactic efficiency of atropine was uncertain in preventing the post-PCB bradycardia.