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Biomedical subjects

L Gluck

Publications and source records attributed to L Gluck.

At least 91 records · Page 5Linked to original sources

Absence of phosphatidylglycerol (PG) in respiratory distress syndrome in the newborn. Study of the minor surfactant phospholipids in newborns.

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.

Asphyxia Neonatorum↗

Phosphatidylinositol and phosphatidylglycerol in amniotic fluid: indices of lung maturity.

The minor phospholipids in amniotic fluid from normal pregnancies were correlated with the well-established index of lung maturity, the lecithin/sphingomyelin (L/S) ratio. When the L/S ratio was less than 1.0, the acidic phospholippids phosphatidylglycerol (PG) and phosphatidylinositol (PI) were absent or low in concentration (0.0 to 2.5 per cent of lipid phosphorus). Parallel to the increase in the L/S ratio to 2.0, the content of PI increased 6.0 to 8.5 per cent of lipid phosphorus. PG, the unique phospholipid of lung surfactant, first appeared and PI concomitantly decreased when the L/S ratio exceeded 2.0, indicating the secretion of mature lung surfactant. Analysis of PI and PG in amniotic fluid as markers of surfactant seems to be of value as an additional index of prenatal evaluation of lung maturity and may be particularly useful when the specimen is contaminated with blood.

Amniotic Fluid↗

Phosphatidylglycerol in lung surfactant. III. Possible modifier of surfactant function.

Lamellar bodies and alveolar lavage from adult mammalian lung contain unusually high concentrations of phosphatidylglycerol that could serve as a sensitive indicator of surfactant. Phosphatidylglycerol was absent and phosphatidylinositol was correspondingly prominent in surfactant from the preterm rabbit fetus. Phosphatidylglycerol rapidly appeared and phosphatidylinositol decreased following the delivery. Surfactant isolated from the prematurely born rabbit or from humans with respiratory distress syndrome never contained phosphatidylglycerol. Comparison between lamellar bodies from fetal and postnatal rabbits revealed remarkably similar composition except for the acidic phospholipids; however, the physico-chemical properties were different. The compressibility of the surface film (i.e. the ratio of the fractional decrease in surface area and the corresponding decrease in surface tension) at low surface tensions was higher with fetal than with postnatal surfactant, whereas the difference in minimum surface tensions was small. These data suggest that phosphatidylglycerol is not an essential component required for the formation of the complex, but it improves the properties of surfactant in stabilizing the alveoli.

Aging↗

Neonatal intensive care in community hospitals and remote areas. The problems and a possible solution.

This has been a brief summary of the problems emerging as more community hospitals develop neonatal intensive care, analyzing their possible origins and significance. A description of one solution to the problem has been given, exemplified by an outreach program from the University of California, San Diego, and University Hospital, San Diego, with the community of Las Vegas, Nevada. We feel strongly that the responsibilities of medical schools toward community hospitals and toward regionalization in isolated communities should be unique and are not covered by usual regulations or traditional concepts of regionalization.

Education, Continuing↗

Preventing obsolescence in the design of a perinatal unit.

Basic principles are offered to support the suggestion that use of special care space must be made with a mind toward prevention of obsolescence. Certain conventional design features should be examined critically and decisions made as to their applicability to the needs of a particular program.

Hospital Design and Construction↗

Phosphatidylglycerol in lung surfactant. II. Subcellular distribution and mechanism of biosynthesis in vitro.

Lamellar inclusion bodies, apparent precursors for alveolar surfactant lining, have remarkably similar phospholipid composition to surfactant from alveolar lavage, but distinctly different from other fractions studied: mitochondria, microsomal fraction containing endoplasmic reticulum membranes, plasma membranes and nuclei. Surfactant contained (as % of total phospholipid phosphate): 75.5-77.0% lecithin, 11.0-11.2% phosphatidylglycerol, 4.2-4.6% phosphatidylethanolamine, 3.0-3.2% phosphatidylinositol, 1.5-1.7% bis-(monoacylglycerol) phosphate, 1.2-1.9% phosphatidylserine, and 0.7-1.5% sphingomyelin. Fatty acids of phosphatidylglycerol from lamellar bodies were similar to those from microsomes but different from those in mitochondria. Lung homogenate in continuous sucrose density gradient displayed two major activity peaks of phosphatidylglycerol synthesis: the heavier from mitochondria; the lighter from endoplasmic reticulum. Studies on mechanism of phosphatidylglycerol synthesis in vitro revealed (in these two fractions) CDP-diglyceride and sn-glycerol phosphate precursors to phosphatidylglycerol phosphate, that hydrolysed to phosphatidylglycerol. In microsomes disaturated CDP-diglycerides were 1.6-1.9 times more active substrates than in mitochondria, whereas CDP-diglycerides from egg lecithin were almost equally active. In contrast to lung mitochondria no cardiolipin synthesis was detected in microsomes. The highest specific activities for phosphatidate cytidyltransferase, CDP-diglyceride-inositol phosphatidyltransferase, choline phosphotransferase, and phosphatidylethanolamine methyltransferase were all found in microsomes. The present in vitro studies and additional evidence (M. Hallman and L. Gluck, (1975) Fed. Proc. 34, 274) support the hypothesis that de novo synthesis of surfactant lecithin phosphatidylinositol and phosphatidylglycerol takes place in the endoplasmic reticulum of alveolar cells.

Animals↗