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Biomedical subjects

Z Friedman

Publications and source records attributed to Z Friedman.

At least 91 records · Page 5Linked to original sources

Cord blood fatty acid composition in infants and in their mothers during the third trimester.

Since essential fatty acids are required for normal brain development, we studied plasma lipids and EFA levels in 16 postpartum mothers (28 to 44 weeks) and in the umbilical vein and artery of 32 newborn infants. Groups of eight 24 to 33-, 34 to 37-, 38 to 42-, and 43 to 44-week-old infants were studied. Plasma fatty acid composition was studied in PL, CE, TG, and FFA by thin-layer and gas-liquid chromatography. Increased values for PL, CE, and TG (P less than 0.001) were noted in maternal plasma compared to cord plasma; linoleic acid was lower (P less than 0.001) in cord plasma PL, CE, and FA. EFA derivatives dihomo-gamma-linolenic, arachidonic, and docosahexaenoic acids were higher in cord plasma (P less than 0.001). Total polyenoic EFA increased with advanced gestation, and at term, was close to maternal levels. delta-5,8,11-eicosatrienoic acid (elevated in EFA deficiency) was elevated in cord plasma as compared with maternal values (P less than 0.001); other criteria of EFA deficiency were absent. These data indicate that fetal EFAs are elongated and desaturated during the third trimester. These higher polyenoic acids may incorporate into lipids in the developing CNS. The lower linoleic acid levels in the fetus may be important to the transplacental transport of EFA.

Brain↗

Digoxin therapy in low-birth-weight infants with patent ductus arteriosus.

Digoxin therapy was evaluated retrospectively in a group of 30, and prospectively in a group of 16 low-birth-weight, premature infants with cardiorespiratory symptoms due to persistent patency of the ductus arteriosus. The response to decongestive therapy was equivocal. Digoxin levels in serum varied between 1.5 and 13 ng/ml. Digoxin half-life in serum exceeded three days in four patients. Fourteen of the combined group of 46 infants had signs of toxicity of digoxin. High dosage, inadvertent overadministration, and variable clearance of digoxin, as well as special characteristics of the patients studied, are postulated as explanations for the high incidence of toxicity. This study suggests that digoxin therapy in low-birth-weight, premature infants with patent ductus arteriosus is not without risk.

Digoxin↗

Urinary excretion of prostaglandin E following the administration of furosemide and indomethacin to sick low-birth-weight infants.

Urinary excretion of prostaglandin E was measured in seven sick low-birth-weight infants. Four had severe hyaline membrane disease and one had chronic bronchopulmonary dysplasia; all received furosemide. Two infants had patent ductus arteriosus and received indomethacin. Following administration of furosemide, urine volume and the excretion rates of sodium and calcium were significantly increased; such changes were not seen following the administration of indomethacin. Prostaglandin E excretion rate was increased from 0.4 +/- 0.04 to 1.3 +/- 0.2 ng/mg Cr (mean +/- SEM) following administration of furosemide, but decreased in two patients following administration of indomethacin. The present results demonstrate that furosemide enhances urinary excretion of prostaglandin E by mechanisms which may reflect an increase in prostaglandin synthesis, a decrease in prostaglandin renal metabolism, or both. Indomethacin, which is a prostaglandin synthetase inhibitor, decreases the urinary excretion of prostaglandin E. These observations suggest that furosemide therapy in patients receiving indomethacin may be ineffective.

Calcium↗

Decreased prostaglandin E turnover in infants with essential fatty acid deficiency.

Sick low birth weight infants (LBWI) are prone to develop rapid onset of essential fatty acid (EFA) deficiency. EFAs serve as precursors for prostaglandins (PGs). We measured the excretion of the major urinary metabolite of prostaglandins E1 and E2, 7alpha-hydroxy-5,11-diketotetranorprostane-1,16-dionic acid (PGE-M), in three EFA-deficient and in nine thriving neonates. There was no significant difference in PGE-M excretion between the sexes among thriving infants nor did PGE-M excretion appear to be affected by postconceptual age. However, a significant difference between the PGE-M excretion in the group of infants with EFA deficiency before and after treatment is apparent (P less than 0.05). Significant differences in PGE-M excretion were also found between the control group and the EFA-deficient infants. The severity of the EFA deficiency correlates directly with the degree of PGs excretion. The biochemical evidences of EFA deficiency and the decreased levels of PGE-M excretion are rapidly corrected when patients resume a diet containing EFA.

Fatty Acids, Essential↗

Essential fatty acids, prostaglandins, and respiratory distress syndrome of the newborn.

The lungs are a major metabolic site for the synthesis, release, and degradation of prostaglandins. Prostaglandins of the E and F series exert a potent physiological effect on the smooth muscle of blood vessels and the tracheobronchial tree; prostaglandin E dilates while prostaglandin F constricts. Thus, altered prostaglandin metabolism may contribute to the pathophysiology of respiratory distress syndrome (RDS). Twenty-one infants with RDS and ten age- and weight-matched controls were studied by analyzing their plasma for prostaglandins and their precursor essential fatty acids. The two groups showed no differences in the essential fatty acid prostaglandin precursors, dihomo-gamma-linolenic and arachidonic acids. During the acute phase of RDS, plasma levels of the primary prostaglandins E and F are significantly elevated compared with control values and the ratio of prostaglandin E to prostaglandin F significantly reduced. Prostaglandins E and F returned to control values on recovery from the acute stage of the disease. Two infants with persistent patent ductus arteriosus had significantly elevated prostglandin E values in their plasma compared with controls. The elevated levels of circulating plasma prostaglandins E and F and the reversal of their ratio during the acute phase of RDS may have adverse pulmonary and multisystem effects.

8,11,14-Eicosatrienoic Acid↗

Furosemide in hyaline membrane disease.

In a randomized clinical trial designed to evaluate the effect of diuresis on infants with hyaline membrane disease, seven infants were treated with furosemide (2 mg/kg intravenously) and five received 5% dextrose water in 0.225% sodium chloride (control group). Arterial blood gas analyses performed before and during the six hours after treatment showed no significant difference between control and treated infants. Urine output and urine sodium and calcium loss were significantly increased (P less than .05) in the infants receiving furosemide. The diuresis seemed to have no effect on left atrial size determined echocardiographically, whereas measurements of dynamic skinfold thickness suggested mobilization of subcutaneous water. One infant became seriously dehydrated and hypotensive secondary to a massive diuresis. We concluded that furosemide had a potent diuretic effect in infants with hyaline membrane disease but does not improve cardiorespiratory function acutely. This may be because of failure to mobilize pulmonary interstitial fluid in the time period tested. It may also be possible that the presence of pulmonary interstitial fluid does not play an important role in the impairment of gas exchange in the acute stage of hyaline membrane disease.

Carbon Dioxide↗

Effect of parenteral fat emulsion on the pulmonary and reticuloendothelial systems in the newborn infant.

Analysis of phospholipids (PL), cholesterol esters, triglycerides (TG), and free fatty acids (FFA) was performed on plasma and RBCs in two sick low-birth-weight infants who received total parenteral nutrition including Intralipid for the first 9 and 12 weeks of life, respectively. There was an increase in the total concentration of the plasma IG and FFA in the infants receiving Intralipid as compared with controls. These elevated lipid levels were not detected by visual inspection of the plasma. When compared with control infants, higher levels of linoleic acid were found in the plasma and RBCs of infants receiving Intralipid while plasma PL contained less arachidonate. Histological examination of the lung in both infants who received Intralipid revealed numerous globules of sudanophilic material in alveolar macrophages and capillaries. There is a possibility that prolonged administration of Intralipid may be associated with altered pulmonary and reticuloendothelial system function.

Cholesterol Esters↗

Elective delivery of the term fetus. An obstetrical hazard.

Of 1,020 consecutive admissions to a regional neonatal center, 38 infants were admitted following elective delivery in which no medical condition of the mother or fetus had necessitated immediate delivery. Twenty infants had problems that were not primarily the result of elective delivery, developed in 18. Fifteen of these 18 infants were delivered by cesarean section; in none of the mothers had any assessment of fetal maturity or size (other than the menstrual history and physical examination) been made. The infants remained in the hospital for an average of 12.7 days at a median cost of $2,678 per patient. One infant died. In the absence of pressing medical indications and without an objective assessment of fetal maturity, elective delivery remains potentially hazardous.

Adult↗

Spongy degeneration of the central nervous system (van Bogaert-Bertrand type?) in a newborn infant. A light and electron microscopic study.

Autopsy findings on a 5 day old infant with hypotonia from birth showed extensive spongy changes of the myelinating tracts within the cerebrum, cerebellum and brain stem. The spongy changes, similar to Van Bogaert-Bertrand disease, resulted from intramyelinic edema. However, unlike the typical forms of this disease, swollen astrocytes with abnormal mitochondria were not found. The relationship of this case to typical forms of Van Bogaert-Bertrand disease is discussed. This case may represent a very early form of Van Bogaert-Bertrand disease or a new pathological entity.

Astrocytes↗

Platelet dysfunction in the neonate with essential fatty acid deficiency.

Platelet aggregation in response to ADP was studied in five EFA-deficient sick premature newborn infants who were receiving fat-free parenteral nutrition. EFA deficiency was diagnosed by analysis of plasma lipid fatty acid values. The deficient infants had impaired platelet aggregation when compared to other low-birth-weight infants fed orally who served as control subjects (maximum 18.1% versus 43.4% at 2.5 muM ADP; 34.5% versus 52.2% at 5.0 muM ADP). In addition, the platelets from EFA-deficient infants demonstrated clearly evident disaggregation. On recovery from their deficient state, the low-birth-weight infants had platelet functions similar to those of apparently healthy premature infants. Clinical hemorrhage occurred in four of the EFA-deficient infants. Thus a deficiency of arachidonic acid, the precursor of thromboxane A2, is correlated with an impairment of the aggregation of platelets, a phenomenon mediated by thromboxane A2. This correlation provides the basis for a hypothesis that the observed EFA deficiency is causally related to the platelet dysfunction.

Adenosine Diphosphate↗

A simple device for reducing insensible water loss in low-birth-weight infants.

Insensible water loss (IWL) was measured in five premature infants, 1 to 4 days old, by multiple weighings on an electronic balance inside an incubator. The babies were studied naked before and after being covered with a transparent thermal blanket. The use of the thermal blanket produced a mean reduction of 70% in IWL and a net caloric saving of 27 kcal/kg/day. There was minimal interference with nursing care. The important caloric saving achieved from reduced vaporization of water and evaporative heat loss may be an important determinant of intact survival in the high-risk infant.

Bedding and Linens↗

Rapid onset of essential fatty acid deficiency in the newborn.

To study the effect of fat-free alimentation on essential fatty acids (EFA), their levels in plasma phospholipids, cholesterol esters, triglycerides, and free fatty acids were measured in five sick newborns. Four patients were under 32 weeks of gestation; three were small for gestational age and one was an infant of a diabetic mother. All developed biochemical evidence of EFA deficiency during the first week of life--the smallest infant did so by the second day. Biochemical evidence of EFA deficiency included a decrease in plasma lipid arachidonic and linoleic acids, an increase in 5,8,11-eicosatrienoic acid, palmitoleic, and oleic acids and a trienoic/tetraenoic ratio of more than 0.4. Oral feeding with EFA reversed these changes. The two infants showing the most severe biochemical evidence of EFA deficiency died. Neither exchange transfusion nor multiple blood transfusions prevented or corrected the development of EFA deficiency. An alternative method for efficient and safe delivery of EFA to such infants is required.

Blood Transfusion↗