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The excretion of C6-C10-dicarboxylic acids, i.e. adipic, suberic and sebacic acids, was measured during the three first days of life in 3 fasting newborns, 2 newborns fed with isocaloric glucose and 2 newborns given mothers'-milk. On the second and third day of life the starved children excreted 27-84 mmol adipic acid/mol creatinine, 6-22 mmol suberic acid/mol creatinine and 4-7 mmol sebacic acid/mol creatinine. The excretion of C6-C10-dicarboxylic acids in the neonates given glucose or mothers'-milk was, for the first three days of life, 0-9 mmol adipic acid/mol creatinine, 0-10 mmol suberic acid/mol creatinine and 0-4 mmol sebacic acid/mol creatinine. The latter amounts are equivalent to the excretion of dicarboxylic acids in older children. It is argued that the detected dicarboxylic acids are formed by omega-oxidation of long-chain monocarboxylic acids followed by beta-oxidation, and that the excreted amounts reflect omega-oxidation activity. It is speculated that the substantial omega-oxidation activity in the starving newborn serve to provide succinyl-CoA-substrate for the citric acid cycle and for gluconeogenesis.
Phosphatidylglycerol (PG) was absent from lung effluent in 41 infants with respiratory distress syndrome of the newborn (RDS), whereas effluent from healthy control subjects of similar gestational age contained this phospholipid (4.9 +/- 2.4% of lipidphosphorus (P), n = 32). Control infants of 28 weeks of gestation or less with various respiratory disturbances other than RDS also had low PG (0.2 +/- 0.2% of lipid-P, n = 5). In RDS surfactant complex often could be isolated from the airways using differential and density gradient centrifugation. The material thus obtained had prominent phosphatidylinositol (PI) (13.6 +/- 2.8% of lipid-P, n = 6), but no PG. Of those 18 infants who had such surfactant even in the early stages of RDS, 13 were 35 weeks of gestation or more, 3 were offspring of diabetic mothers, and 2 had severe perinatal asphyxia. In healthy control subjects PG sometimes appeared first within an hour of birth, but in RDS PG did not appear until recovery from RDS. In RDS type II (transient tachypnea of the newborn) PG in lung effluent also was abnormally low (1.3 +/- 0.6% of lipid-P, n = 5) and PI was correspondingly prominent (9.7 +/- 3.6% of lipid-P, n = 5), indicating immaturity of surfactant similar to RDS. Surfactant with PG and PI has superior surface-active properties compared to that containing PI, but no PG. Surfactant without PG does not seem to stabilize the alveoli of the newborn as well as does surfactant with PG. The failure of PG appearance following birth therefore may precipitate RDS, especially beyond 35 weeks of gestation.
Eighty-five cardiotachograms of newborns aged between 34 and 42 weeks of gestation were studied. Fifty newborns were delivered spontaneously. In seventeen cases caesarean sections were used and in eighteen cases vacuum extractions. Cardiotachograms were recorded continuously throughout the immediate postnatal period until the stabilisation of the heart rate. Cardiotachograms were divided into three typical groups based on their cours of heart rate and fluctuation. The relation between these groups and the methods and duration of delivery and the condition of newborns were discussed. We found a correlation between the pathological cardiotachograms (tachycardiac and bradycardiac type of cardiotachogram) and long expulsion time, existent history of intrauterine disorder and low Apgar score. No relationship could be established between pathological cardiotachograms and the method of delivery.
Five newborn girls presented with small intestinal obstruction and microcolon and a giant bladder (megacystis). Organic causes of obstruction were not found, and the gastrointestinal tract failed to function after appropriate diversion. Two died in the postoperative period, two lived several months on central venous hyperalimentation, and one died at 34 months of age following chronic though intermittent hyperalimentation. Pathologic studies showed an abundance of ganglion cells in both dilated and narrowed areas of intestine; the combined small bowel-colon length was one-third of normal in the absence of an evident obstructive or vascular insult. The five patients represent the most severe manifestation of defective intestinal peristalsis in a larger group of distended newborns in whom organic gastrointestinal obstruction is not found. Treatment with central venous hyperalimentation may sustain life, and some patients eventually recover gastrointestinal function. The hypoperistalsis is largely refractory to pharmacologic treatment; its cause is unknown.
Fourteen term newborn infants have been recognized as having transient tricuspid insufficiency associated with significant perinatal stress. Five of these infants underwent cardiac catheterization for presumed congenital heart disease, but had only massive tricuspid valve insufficiency. The other nine infants were diagnosed on the basis of a murmur characteristic of tricuspid valve insufficiency and on other clinical grounds. All had a history of significant perinatal stress in the form of asphyxia with or without hypoglycemia. Frequently, congestive heart failure, persistent cyanosis, and ECG evidence of myocardial ischemia were present. Twelve of the 14 survived, and in each of them all cardiac signs and symptoms, including the murmur, spontaneously resolved. The two patients who died had histopathologic evidence of necrosis in the anterior papillary muscle of the tricuspid valve. The constant features of perinatal stress, ST-T wave abnormalities on the ECG, and spontaneous resolution of the transient tricuspid insufficiency strongly suggest that this syndrome is secondary to a reversible form of myocardial dysfunction, perhaps by affecting papillary muscle specifically. We believe that hypoxia with or without hypoglycemia precipitates the events leading to this clinical syndrome which is distinguishable from other cardiac abnormalities in the newborn by the history, distinctive murmur, and the ECG abnormalities.
Evidence has already been adduced suggesting that an increase in microtubular number occurs in the tractus hypophyseus of rats stressed by the administration of hypertonic saline, and of rats with congenital diabetes insipidus (CDI). Since the tractus hypophyseus in these animals shows high secretory activity, it seems likely that the microtubular increase reflects the participation of microtubules in axoplasmic transport. To exclude, however, a congenital microtubular abnormality in CDI, affected newborn rats were examined. In these, the microtubular number was normal, thus suggesting that the increase in microtubular number seen in adult animals was not a congenital morphological abnormality. However, by 4 days of age there was a slight but statistically significant increase in microtubular number in affected rats, a change probably attributable to increased secretory activity.
Ten term and eleven preterm newborn infants with appropriate weights for their gestational age were infused for one minute with L-alanine (150 mg/kg) at the age of 29 to 76 hours (mean 48 hours) and circulating levels of glucose, lactate, pyruvate, D-betahydroxybutyrate (D-BOHB), insulin and glucagon were monitored. Plasma glucose concentrations increased from 2.7 +/- 0.16 (mean +/- S.E.M.) to 3.7 +/- 0.2 mmol/l after 50 min (p less than 0.01) in term infants. In preterm infants, after an initial decrease of the glucose level from 3.1 +/- 0.16 to 2.6 +/- 0.16 mmol/l (p less than 0.05), it returned to the baseline level at 50 min: 3.0 +/- 0.2 mmol/l. The blood concentration of D-BOHB decreased in term infants from 192 +/- 37 to 112 + 6 micrometer/l (p less than 0.01) after 40 min. In preterms, its decrease was not significant (p greater than 0.05). Plasma glucagon level rose from 53 +/- 5 to 70 +/- 8 pmol/l after ten minutes (p less than 0.01) in terms infants and from 61 +/- 6 to 75 +/- 9 after 20 min (p less than 0.01) in preterm infants. There were no significant changes in plasma insulin concentrations in either group. Forty minutes after L-alanine infusion, I/G ratios were lower in preterm infants (1.26 +/- 0.14) than in term infants (1.71 +/- 0.25) (p less than 0.01). There was no relationship between the glycemic responses to L-alanine and the basal levels of D-BOHB. The data suggest that the glycemic effect of L-alanine infusion and circulating glucagon depends upon a specific stage in maturation. The antiketogenic effect of L-alanine infusion is observed in term infants as in adults.
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