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Biomedical subjects

J B Warshaw

Publications and source records attributed to J B Warshaw.

At least 73 records · Page 4Linked to original sources
PubMed1979

Thyrotropin-releasing hormone increases the amount of surfactant in lung lavage from fetal rabbits.

UNLABELLED: Administration of thyrotropin-releasing hormone (TRH) to pregnant rabbits at 25 and 26 days of gestation results in increased pulmonary surfactant production by the fetus at 27 days (full term is 31 days). There was 60% more total phospholipid and 150% more phosphatidylcholine (the major component of surfactant) in the lung lavage from the fetuses in the treated group than in that from the controls. Lung lavage from the fetuses in the treated litters contained 13.4 +/- 1.6 micrograms of total phospholipid phosphorus/g lung dry wt and 5.6 +/- 1.1 micrograms of phosphatidylcholine phosphorus while that from the fetuses in the control litters contained only 8.2 +/- 1.1 micrograms and 2.2 +/- 0.4 micrograms, respectively. The phosphatidylcholine/sphingomyelin ratio increased from 1.0 in the lavage from the controls to 2.2 in that from the treated group. These changes in lung lavage phospholipid content and composition are in the direction of increased lung maturation. TRH administration had no effect on the incorporation of choline into phosphatidylcholine in fetal lung slices. These data suggest that TRH stimulates surfactant release rather than synthesis. SPECULATION: TRH has a physiologic role in fetal lung maturation and surfactant production. It may potentially be used in the prevention of the respiratory distress syndrome in humans.

Animals↗
PubMed1979

Relevance of the gestational age distribution of meconium passage in utero.

The incidence of meconium staining of the amniotic fluid among the admissions to a newborn special care unit was determined. Meconium staining of the amniotic fluid was present in 251 (7.5%) of 3,374 admissions. The majority of those with meconium staining (98.4%) was of 37 weeks gestation or greater and none was less than 34 weeks gestation. The possible relevance of this gestational age distribution is discussed.

Amniotic Fluid↗
PubMed1978

Development of glycogen and phospholipid metabolism in fetal and newborn rat lung.

Glucose, a major metabolic substrate for the mammalian fetus, probably makes significant contributions to surface active phospholipid synthesis in adult lung. We examined the developmental patterns of glycogen content, glycogen synthase activity, glycogen phosphorylase activity and glucose oxidation in fetal and newborn rat lung. These patterns were correlated with the development of phosphatidylcholine synthesis, content and the activities of enzymes involved in phosphatidylcholine synthesis. Fetal lung glycogen concentration increased until day 20 of gestation (term is 22 days) after which it declined to low levels. Activity of both glycogen synthase I and total glycogen synthase (I + D) in fetal lung increased late in gestation. Increased lung glycogen concentration preceded changes in enzyme activity. Glycogen phosphorylase a and total glycogen phosphorylase (a + b) activity in fetal lung increased during the period of prenatal glycogen depletion. The activity of the pentose phosphate pathway, as measured by the ratio of CO2 derived from oxidation of C1 and C6 of glucose, declined after birth. Fetal lung total phospholipid, phosphatidycholine and disaturated phosphatidylcholine content increased by 60, 90 and 180%, respectively, between day 19 of gestation and the first postnatal day. Incorporation of choline into phosphatidylcholine and disaturated phosphatidylcholine increased 10-fold during this time. No changes in phosphatidylcholine enzyme activities were noted during gestation, but both choline phosphate cytidylyltransferase and phosphatidate phosphatase activity increased after birth. The possible contributions of carbohydrate derived from fetal lung glycogen to phospholipid synthesis are discussed.

Aging↗
PubMed1978

Amelioration of bronchopulmonary dysplasia after vitamin E administration. A preliminary report.

We studied the effect of vitamin E on the development of bronchopulmonary dysplasis in neonates with respiratory-distress syndrome. Twenty infants received vitamin E administered intramuscularly during the acute phase of the syndrome, and 20 infants served as controls. Administration of vitamin E significantly increased the serum vitamin E concentration. Nine vitamin-treated and 13 control patients required supplemental oxygen for longer than 250 hours; all were treated with positive-pressure ventilation and endotracheal continuous distending airway pressure. Six of those 13 controls had x-ray changes consistent with bronchopulmonary dysplasia, and four died. None of the nine vitamin-treated patients had changes characteristic of bronchopulmonary dysplasia (P = 0.046), and all survived. Administration of vitamin E during the acute phase of the respiratory-distress syndrome appears to modify the development of bronchopulmonary dysplasis.

Bronchial Diseases↗
PubMed1978

The relationship between premature rupture of the membranes and the respiratory distress syndrome. An update and plan of management.

The records of 340 infants of 36 weeks' gestational age or less were reviewed to study the relationship between premature rupture of the membranes (PRM) and the development of the respiratory distress syndrome (RDS). Twins and infants of diabetic mothers were excluded from the data analysis. PRM of 16 hours or more was associated with statistically significant reduction in the incidence of RDS in infants of 31 weeks' gestational age and older. The association between PRM in excess of 16 hours and survival, however, was only statistically significant for infants of 33 weeks' gestational age and older. The implications of these results and a proposed plan of management for premature infants with PRM are discussed.

Female↗
PubMed1977

Determination of optimal continuous positive airway pressure for the treatment of IRDS by measurement of esophageal pressure.

We describe a simple and reliable method to determine optimal airway pressure in infants with idiopathic respiratory distress syndrome who require continuous positive airway pressure treatment. Esophageal pressure was monitored in ten infants with IRDS during initial application of CPAP. As the level of CPAP was increased in 2 cm H2O increments, changes in Pes were compared with changes in PaO2. Below optimal airway pressure, Pes as well as PaO2 increased insignificantly. When optimal airway pressure (8.1 +/- 0.8 cm H2O) was applied, there was a marked increase in Pes (3.6 +/- 0.8 cm H2O. p less than 0.001) and PaO2 (39.0 +/- 10.0 mm Hg, p less than 0.01). Further increase in CPAP did not result in any subsequent appreciable increase in Pes while PaO2 decreased slightly and PaCO2 increased. Less than optimal CPAP increases F102 requirements and may increase the associated risk of bronchopulmonary dysplasia, while excessive levels of CPAP may increase the risk of pneumothorax. We suggest that esophageal pressure be monitored routinely to determine the optimal level of CPAP for each infant during the initial application of therapy.

Carbon Dioxide↗
PubMed1977

Neonatal red cell superoxide dismutase enzyme levels: possible role as a cellular defense mechanism against pulmonary oxygen toxicity.

Red cell superoxide dismutase (SOD) enzyme activity was determined in 58 cord blood specimens obtained from infants over a range of gestational ages. An inverse relationship between red cell SOD activity and gestational age was demonstrated. Red cell SOD activity showed a progressive fall from 263.1 +/- 30.5 units/mg non-hemoglobin protein (NHP) in infants of less than 29 weeks of gestation to 168.9 +/- 21.3 units/mg NHP in infants of more than 36 weeks of gestation (P less than 0.05). Infants treated for RDS showed an increase in red cell SOD activity which reached significance at 72 hr when compared to cord blood levels from the same population (P less than 0.05). No similar significant difference could be demonstrated in gestational age-matched control subjects over the same time period. However, initial cord blood SOD enzyme levels were lower in premature infants with RDS (229.5 +/- 30.6 units/mg NHP) than in premature infants without RDS (264.0 +/- 38.0 units/mg NHP). When infants with RDS were examined for oxygen toxicity and survival, red cell SOD levels were noted to decrease over 24 hr in four of five infants who died, three of whom developed bronchopulmonary dysplasia. In the surviving infants, red cell SOD levels showed a significant increase by 48 hr (P less than 0.05). None developed bronchopulmonary dyplasia and all survived.

Bronchial Diseases↗
PubMed1976

A comparison of early-onset group B streptococcal neonatal infection and the respiratory-distress syndrome of the newborn.

In attempting to differentiate early-onset Group B streptococcal infection from hyaline-membrane disease we found features of severe Group B infection to be rupture of the membranes for more than 12 hours before delivery (four or eight versus one of nine), gram-positive cocci in the gastric aspirate (four or four versus none of one), apnea and shock in the first 24 hours of life (seven of eight versus none of nine), and the generation of lower peak inspiratory pressures on avolume-cycled respirator (mean of 36.5 +/- 2.8 versus 63.9 +/- 6.2 cm of water; P = 0.005). In eight fatal cases of Group B infection, four patients had radiographic features indistinguishable from hyaline-membrane disease whereas the other cases were consistent with neonatal pneumonia. Seven of the eight infected infants had no histologic evidence of coexisting hyaline-membrane disease. Microscopical features of Group B infection included cocci in unevenly distributed hyaline membranes and minimal atelectasis. Group B streptococcal infection differs clinically and pathologically from hyaline-membrane disease. Differentiating clinical features include early apnea and shock and lower inspiratory pressures on mechanical ventilation.

Diagnosis, Differential↗
PubMed1976

Importance of radiant flux in the treatment of hyperbilirubinemia: failure of overhead phototherapy units in intensive care units.

Prior to 1972, radiation used to treat neonatal hyperbilirubinemia was based upon the photometric unit, the foot-candle, a measure of light illumination. Measurements in terms of microwatts per square centimeter for selective wavelengths is more precise. We compared the effectiveness of phototherapy provided by overhead phototherapy units in intensive care modules vs. conventional phototherapy units. Forty-two infants were studied over a six-month period and divided into three groups based upon radiant flux measurements as follows: Group 1 (No. = 6), 1.0 muw to 1.9 muw/sq cm/nm; group 2 (No. = 15), 2.0 muw to 3.9 muw/sq cm/nm; group 3 (No. = 21), 4.0 muw to 6.0 muw/sq cm/nm. All flux determinations were made within the 400- to 500-nm range. All infants in group 1 were treated with overhead phototherapy units in the intensive care modules. Because of multiple factors known to increase the risk of kernicterus, evaluation of effectiveness of phototherapy at low radiant flux was limited in group 1. Significant changes in bilirubin were noted by 48 hours when comparing group 3 with groups 1 and 2. A minimum of 4.0 muw/sq cm/nm appears necessary for effective phototherapy. As designed, phototherapy units in intensive care modules are ineffective in delivering this therapeutic level of radiant flux.

Humans↗