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Biomedical subjects

M Hallman

Publications and source records attributed to M Hallman.

At least 181 records · Page 10Linked to original sources
PubMed1982

Evidence of lung surfactant abnormality in respiratory failure. Study of bronchoalveolar lavage phospholipids, surface activity, phospholipase activity, and plasma myoinositol.

Autopsy findings suggest that lung surfactant is damaged in the adult respiratory distress syndrome. In the present study 225 bronchoalveolar lavage specimens (78 from 36 patients, 1-78 yr old with respiratory failure, 135 from another 128 patients with other respiratory disease, and 12 from healthy controls) were assayed for the lung profile [lecithin/sphingomyelin (L/S) ratio, saturated lecithin, phosphatidylinositol, and phosphatidylglycerol]. Bronchoalveolar lavage fluid was further analyzed for phospholipids and for phosphatidic acid phosphohydrolase, phospholipase A2, and phosphatidylinositol phosphodiesterase activities. A lipid-protein complex was isolated and analyzed for surface activity, and plasma was measured for myoinositol. There were only small differences seen in the recovery of total phospholipid between respiratory failure patients and normal controls. However, in respiratory failure, phospholipids in bronchoalveolar lavage were qualitatively different from those recovered either from normal controls or from patients with other lung disease: the LO/S ratio, phosphatidylglycerol, and disaturated lecithin were low, whereas sphingomyelin and phosphatidylserine were prominent. These abnormalities were present early in respiratory failure and tended to normalize during recovery. Low L/S ratio (less than 2), and low phosphatidylglycerol (1% or less of glycerophospholipids) in bronchoalveolar lavage was always associated with respiratory failure. Abnormal lavage phospholipids were not due to plasma contamination. The phospholipase studies revealed little evidence of increased catabolism of phospholipids. In respiratory failure, the lipid-protein complexes from lung lavage were not surface active, whereas that from healthy controls had surface properties similar to lung surfactant. Phospholipids from patients with respiratory failure were similar to those from respiratory distress syndrome in the newborn. However, the latter condition is characterized by fast recovery of surfactant deficiency and by high plasma myoinositol that suppresses the synthesis of surfactant phosphatidylglycerol and increases phosphatidylinositol (Pediatr. Res. 1981. 15: 720). On the other hand, in adult respiratory distress syndrome, the abnormality in surfactant phospholipids may last for weeks and in most cases is associated with low phosphatidylinositol, low phosphatidylglycerol, and low plasma myoinositol.

Adult↗
PubMed1982

Lung surfactant phospholipids in the foetus, newborn, and in the adult; evidence of abnormality in respiratory failure.

The surface active material on the peripheral airway lining prevents atelectasis and its consequences. Abnormalities in lung surfactant can be diagnosed by analysis of the amniotic fluid in the foetus, tracheal aspirate in the newborn, and segmental bronchoalveolar lavage in children or adults. In the respiratory distress syndrome in the newborn (RDS) surfactant phospholipids are immature. This is a major cause of respiratory failure in RDS. In acute respiratory failure in adults and in children (ARF) alveolar phospholipids are abnormal. There are three main types of surfactant abnormalities; 1) Immature surfactant in RDS, 2) defective surfactant phospholipids in ARF, and 3) inhibition of surfactant function by proteins (mostly due to increased alveolar permeability) in RDS, ARF, and in alveolar proteinosis. The importance of myoinositol in surfactant metabolism is discussed.

Adult↗
PubMed1981

Measurement of the lecithin/sphingomyelin ratio and phosphatidylglycerol in aminotic fluid: an accurate method for the assessment of fetal lung maturity.

A total of 506 amniotic fluid samples from 337 pregnancies was analysed for lecithin/sphingomyelin (L/S) ratio and phosphatidylglycerol. Two-dimensional chromatography on either laboratory-made or commercial thin-layer silica gel plates was required for proper resolution of the phospholipids. The predictive accuracy of the L/S ratio and the phosphatidylglycerol analysis was assessed in 225 patients, 187 of whom had an L/S ratio of 2 or more. In addition to predicting respiratory distress syndrome of the newborn, the phospholipid results predicted the risk of transient tachypnoea, symptomatic pneumothorax and the persistence of fetal circulation. The phosphatidylglycerol results improved the predictive value of both the mature L/S ratio (2 or more) and the non-mature L/S ratio (below 2).

Amniotic Fluid↗
PubMed1981

Analysis of labeling and clearance of lung surfactant phospholipids in rabbit. Evidence of bidirectional surfactant flux between lamellar bodies and alveolar lavage.

Turnover and clearance of lung surfactant phospholipids were studied with particular reference to myoinositol-induced perturbation in the acidic phospholipids. Administration of myoinositol decreased [(3)H]palmitate and [(32)P]phosphate incorporation into phosphatidylglycerol by 80-90% in whole lung, and by 94-99% in lamellar bodies and in alveolar lavage. The increased incorporation of radioactive isotopes into phosphatidylinositol following myoinositol, was inverse to the decrease in phosphatidyl-glycerol incorporation. Myoinositol treatment affected neither content nor labeling of phosphatidylcholine or disaturated phosphatidylcholine as studied within 50 h of administration. Phosphatidylglycerol was pulse labeled by intravenous [(32)P]phosphate and [(3)H]palmitate, followed by myoinositol. The biological half-lives of phosphatidylglycerol in the microsomal fraction, lamellar bodies, and alveolar lavage were 1.6, 4.6, 5.4 h (with (3)H), and 2.8, 6.5, 7.0 h (with (32)P), respectively.(32)P-labeled lung surfactant tracer was applied to the airways in saline suspension and the clearance of phospholipid radioactivity was measured in alveolar lavage, alveolar macrophages, lamellar bodies and lung homogenates. The clearance rates of phosphatidylcholine, disaturated phosphatidylcholine, phosphatidylglycerol, and phosphatidylinositol as studied in whole lung over 6 h were 3.4-5.8% h. Only a small amount of phospholipid radioactivity was recovered in the alveolar macrophage fraction (including bis-[monoacylglycerol]phosphate). Phospholipid radioactivity in alveolar lavage fell to 40-70% of the maximum during the 1st h, and to 5-18% over the next 6 h. During 2 h after the application of phospholipids, the radioactivity in the lamellar body fraction increased, and the specific radioactivities approached those in alveolar lavage. The association of phosphatidylglycerol with lamellar bodies was unaffected by myoinositol. Phosphatidylinositol entered more slowly than did phosphatidylglycerol from microsomes to the alveolar lavage fraction, and from alveolar lavage to lamellar bodies. These differences may be of importance regarding the poor performance of phosphatidylinositol-containing surfactant at birth. Further investigations are needed to clarify the possible role for the postulated bidirectional surfactant flux between the lamellar body and alveolar lavage fractions in maintaining the activity of surfactant.

Animals↗
PubMed1980

Evidence of surfactant deficiency in persistence of the fetal circulation.

The phospholipids of tracheal aspirates in persistence of the fetal circulation (PFC) were compared to those in the respiratory distress syndrome (RDS) and those in other severe diseases of the newborn. The infants with PFC were hypoxemic despite 80 to 100% inspiratory oxygen. There were small, if any, pulmonary parenchymal changes in radiographs. Echocardiograms demonstrated evidence of increased pulmonary arterial pressure. Mechanical ventilation increased arterial oxygen tension in each case. However, five of the eight patients required ventilation at a high frequency (57-65 min) and long inspiratory time (0.6--0.7 s). The phospholipids in tracheal aspirates in PFC were quite similar to those in RDS, namely there was a small amount, if any, phosphatidylglycerol (PG), and the lecithin/sphingomyelin (L/S) ratio was low. However, phosphatidylinositol was higher in PFC than in RDS. In the other diseases studied, the phospholipid composition resembled that of the normal newborn, namely PG was present and the L/S ratio was high. Surfactant deficiency seems to be important in the pathogenesis of some cases of PFC. The favorable effect of mechanical ventilation may be partly due to the stabilization of peripheral airways.

Echocardiography↗
PubMed1980

Maternal glucocorticoid in unplanned premature labor. Controlled study on the effects of betamethasone phosphate on the phospholipids of the gastric aspirate and on the adrenal cortical function of the newborn infant.

The effects of betamethasone on surfactant composition and neonatal adrenal function were compared with placebo in a double-blind study, which included 74 patients at risk for premature delivery. The overall incidence of respiratory distress syndrome was low, and no differnce was observed between the betamethasone and placebo groups. The phospholipid pattern (lecithin/sphingomyellin ratio, acetone precipitated lecithin, phosphatidylinositol/sphingomyelin ratio, and phosphatidylglycerol/sphingomyelin ratio) from gastric aspirates of newborn infants was similar in the betamethasone and placebo groups, suggesting a similarity in lung surfactant. The responsiveness of the adrenal cortex of the newborn infants, evaluated by a 2-hr adrenocorticotropic hormone test at the age of 24 hr, did not differ between infants whose mothers had received either betamethasone or placebo. The low incidence of respiratory distress syndrome in the betamethasone and placebo groups was ascribed in part to a high incidence of prolonged rupture of fetal membranes. Our results do not exclude the possibility that antenatal maternal administration of betamethasone could prevent respiratory distress syndrome in other defined high-risk infants.

Adrenal Cortex↗
PubMed1980

Phospholipid studies of the amniotic fluid in diabetic pregnancy.

The lecithin/sphingomyelin ration (L/S) of the amniotic fluid is a reliable indicator of fetal lung maturity in most disorders complicating pregnancy. False positive results of L/S occur especially in diabetic pregnancies. Phosphatidylglycerol (PG) improves the ability of the surface active lecithin to prevent lung atelectasis. Respiratory distress syndrome of the newborn infant does not seem to occur when PG is present. By determining PG of the amniotic fluid, false positive L/S can be excluded in diabetic pregnancies.

Amniotic Fluid↗
PubMed1979

Amniotic fluid phospholipid profile as a predictor of fetal maturity in diabetic pregnancies.

The phospholipids in amniotic fluid from diabetic pregnancies were compared with those in normal pregnancies. There was little difference in the lecithin/sphingomyelin (L/S) ratios on the basis of the gestational ages. However, in diabetic pregnancies, phosphatidylglycerol (PG) was absent or low, and phosphatidylinositol (PI) remained high even if the L/S ratio was greater than 2. The phosphatidylglycerol/phosphatidylinositol (PG/PI) ratio was expressed as a function of the L/S ratio. The PG/PI ratio was significantly lower in maternal diabetes. Respiratory distress syndrome (RDS) coincided with an L/S ratio of between 2.0 and 3.0 only when PG was absent. Infants of insulin-dependent diabetic mothers with a particularly low PG/PI ratio (less than 50% of the median) had higher relative birth weights and more often had hypoglycemia than those infants born to mothers with a high PG/PI ratio (greater than 200% of the median). The phospholipids of amniotic fluid correlate with fetal functional maturity and may reflect deviations of hormonal balance required for normal perinatal development.

Amniotic Fluid↗
PubMed1977

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↗