Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five patients with neurogenic pulmonary edema (NPE) were reported. The edemas were caused by head injuries in four patients and by a craniotomy in the fifth. The onset of NPE was either acute (3 hours after injury) or was slow to develop (4 days later). Clinical symptoms included the sudden onset of coughing, tachypnea, tachycardia, and pink bubbly sputum. Moreover, the patients also suffered cyanosis, confusion, or respiratory failure. The distribution of the resulting pulmonary edema was diffuse in 4 cases and localized within a single lobe of the lung in 1 case. Treatment of the NPE included reducing intracranial pressure (glycerol), diuresis (furosemide and mannitol), narcotics (morphine, phenobarbital), and blocking the peripheral effect of sympathetic reflex activity (hydralazine, sodium nitroprusside). Mechanical ventilation support (CPU-1) in combination with controlled hyperventilation may also be necessary. The inability to correct hypoxemia without toxic levels of oxygen necessitates the use of PEEP (positive end-expiratory pressure, +5-10 cmH2O). Resolution of symptoms was noted 24 to 48 hours after treatment in 4 patients. Early diagnosis and intensive care of the pulmonary edema may have a significant bearing on the recovery of lung functions. Unfortunately, 4 of the patients failed to survive because of central nervous system failure. We therefore want to emphasize that NPE can cause secondary deterioration of neurological functions. In conclusion, when dealing with respiratory distress patients with CNS injuries, the possibility of additional damage from a NPE must be taken into consideration.
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PMID:[Neurogenic pulmonary edema: five cases report]. 129 67

Since hyaline membrane disease (HMD) is an important cause of mortality and morbidity in preterm newborns, we decided to evaluate the utility of pulmonary phospholipid (PP) determination in gastric aspirate for confirmatory diagnosis. For that purpose we studied 31 preterm and 30 term babies and compared the results between them and PP in gastric aspirate and amniotic fluid from their mothers. All the term newborns were normal, with mean weight of 3,221, and 39 weeks of gestational age; the results of phosphatidyl inositol (PI) and phosphatidyl glycerol (PG) were positive. The premature babies had a mean weight of 2,424 g and 35 weeks of gestational age. Thirteen had respiratory distress, 4 transient tachypnea and 9 HMD. In this group the babies with PI present and PG absent developed respiratory distress without HMD. The test had sensibility of 69% and specificity of 100%, and in patients without PG and PI the sensibility and specificity was 100%. We concluded that this test has enough sensibility and specificity for the confirmation of HMD in gastric aspirate when the PI and PG are not present.
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PMID:[The determination of pulmonary phospholipids in the gastric contents for an assessment of the respiratory distress syndrome]. 163 9

Platelet-activating factor (PAF) represents a group of phospholipids with the basic structure of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine. A number of different cells are capable of producing PAF in response to various stimuli. The initial step of PAF formation is activation of phospholipase A2 in a calcium-dependent manner, yielding lyso-PAF. During this step arachidonic acid is also released and can be converted to its respective cyclooxygenase and lipoxygenase products. The lyso-PAF generated is then acetylated in position 2 of the glycerol backbone by a coenzyme A (CoA)-dependent acetyltransferase. An additional pathway may exist whereby PAF is generated de novo from 1-alkyl-2-acetyl-sn-glycerol by phosphocholine transferase. PAF inactivation in cells and blood is by specific acetylhydrolases. PAF exhibits a variety of biological activities including platelet and leukocyte aggregation and activation, increased vascular permeability, respiratory distress, decreased cardiac output, and hypotension. In the kidney PAF can produce decreases in blood flow, glomerular filtration, and fluid and electrolyte excretion. Intrarenal artery injection of PAF may also result in glomerular accumulation of platelets and leukocytes and mild proteinuria. PAF increases prostaglandin formation in the isolated kidney and in cultured glomerular mesangial cells. PAF also causes contraction of mesangial cells. Upon stimulation with calcium ionophore the isolated kidney, isolated glomeruli and medullary cells, and cultured mesangial cells are capable of producing PAF. The potential role for PAF in renal physiology and pathophysiology requires further investigation that may be complicated by 1) the multiple interactions of PAF, prostaglandins, and leukotrienes and 2) the autocoid nature of PAF, which may restrict its action to its site of generation.
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PMID:Platelet-activating factor and the kidney. 308 26

Two currently used methods of determining fetal pulmonary maturity were verified on the basis of 148 amniotic fluid samples: one dimensional sequential thin-layer chromatographic determination of the lecithin: sphingomyelin ratio and of phosphatidyl glycerol, and an immunologic slide detection of phosphatidyl glycerol (Amniostat-FLM). With both methods, which have the advantage that they can be performed quickly and can sometimes even be used at the bedside (Amniostat-FLM), a respiratory distress syndrome in the newborn can be ruled out with a high degree of confidence if the threshold values are exceeded (L/S greater than 2; phosphatidyl glycerol present). As with all historical methods, the positive correctness of these two modern methods (no RDS if the child is born within 72 hours despite a negative phosphatidyl glycerol test in the amniotic fluid) is low. Clearly, apart from the quantitative existence of certain surfactant phospholipids (lecithin, phosphatidyl glycerol), there are other perinatal events or measures which determine the extent and severity of RDS in the immature newborn.
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PMID:[Current methods of prenatal determination of lung maturity of the infant from amniotic fluid]. 336 21

We present here a combined, quantitative enzymatic procedure for determining amniotic fluid phosphatidylglycerol and phosphatidylcholine and relate these findings to the assessment of fetal lung maturity. Under the assay conditions described phospholipase C specifically hydrolyses phosphatidylglycerol (PG) and phosphatidylcholine (PC) but not sphingomyelin, precluding the need for removal of sphingomyelin prior to analysis. Solvent extraction of the phospholipids from the amniotic fluid is, however, employed to avoid spurious elevation of PG and PC results by endogenous glycerol and choline. Of 45 amniocentesis fluids examined, 28 yielded detectable PG concentrations (greater than 0.5 mumol/l) and all but three of these exhibited PC concentrations in excess of 10 mumol/l. One case of respiratory distress occurred in an infant of 29 wk gestation with severe intrauterine growth retardation. Of the remaining 17 fluids in which PG was undetected enzymatically (less than or equal to 0.5 mumol/l), 14 also contained PC concentrations less than or equal to 10 mumol/l and all six cases of true respiratory distress syndrome came from within this sub-group. Strong correlations between the PC concentration and the lecithin:sphingomyelin ratio, r = 0.85 (p less than 0.001) and the PC and PG concentrations, r = 0.96 (p less than 0.001) were also found.
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PMID:Combined enzymatic assay of phosphatidylglycerol and phosphatidylcholine in amniotic fluid. 337 Aug 19

The increased incidence of the idiopathic respiratory distress syndrome (IRDS) in infants of diabetic mothers may be explained by preterm delivery and asphyxia but the metabolic derangement per se may also be responsible for the inadequate production of surfactant. Experimental studies of the underlying mechanisms in the lungs of fetuses of pregnant diabetic rats have shown a decreased formation of the two major surfactant phospholipids disaturated phosphatidyl choline and phosphatidyl glycerol. In addition, the activities of key enzymes responsible for the production of these phospholipids are decreased in the fetal lung tissue. Inadequate utilization of pulmonary glycogen for surfactant biosynthesis has also been observed. Furthermore, experimental studies support that other changes than fetal hyperinsulinaemia are needed to produce a state of disturbed surfactant production. In human diabetic pregnancy strict metabolic control allows the fetal lungs to mature in a near-normal fashion. The presence of phosphatidyl glycerol in the amniotic fluid seems to be the best available predictor of lung maturity in diabetic pregnancy, in which both the lecithin/sphingomyelin ratio and amniotic fluid cytology may result in false-positive and false-negative values. The trend towards extension of delivery to term will undoubtedly diminish the need for estimation of fetal lung maturity by amniocentesis. Avoiding preterm delivery and adhering to strict metabolic control of the maternal diabetes would be expected to decrease the neonatal respiratory problems in diabetic pregnancy.
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PMID:Fetal lung maturation in diabetic pregnancy. 346 44

Phosphatidylglycerol (PG) was extracted from 54 human amniotic fluids for the assessment of fetal lung maturity. The PG values were derived from an enzymatic assay involving initial conversion of PG to glycerol by phospholipase C and alkaline phosphatase with subsequent analysis of the glycerol formed. This method proved to be reliable when compared with a method for two-dimensional thin layer chromatographic (2D TLC) analysis of amniotic fluid phospholipids. The results revealed that in all but one of 27 amniotic fluids in which no PG was detected by 2D TLC, enzymatic PG concentrations were less than or equal to 1.5 mumol/l and out of these, from 10 newborn infants delivered within 72 h of sampling, 4 developed respiratory distress syndrome (RDS). Conversely, in all but one of 27 amniotic fluids found to contain PG by 2D TLC, enzymatic PG concentrations were greater than 1.5 mumol/l and except for one subject from non-identical twins, no infants developed RDS.
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PMID:Quantitative determination of phosphatidylglycerol in amniotic fluid by enzymatic assay. 405 5

The lungs of fetuses of streptozotocin-diabetic rats were examined for their ability to incorporate U-14C-glucose into phosphatidyl choline, phosphatidyl glycerol, phosphatidyl inositol and lysophosphatidyl choline. In the lungs of control rats an increased biosynthesis of phosphatidyl glycerol in late pregnancy suggested a close association between the production of this phospholipid and the terminal maturation of the fetal lung. In the offspring of diabetic rats the incorporation of 14C-glucose into phosphatidyl choline, lysophosphatidyl choline and phosphatidyl glycerol was markedly decreased compared with the control rats on gestational day 20, whereas no difference was seen at day 22. Insulin treatment of the pregnant rats restored the biosynthesis of phosphatidyl choline and lysophosphatidyl choline towards normal on gestational day 20, while the ratio of phosphatidyl glycerol to phosphatidyl inositol incorporation of 14C-glucose was decreased, suggesting that the biosynthesis of phosphatidyl glycerol is more sensitive than that of phosphatidyl choline and lysophosphatidyl choline to the metabolic disturbances inherent in maternal diabetes. The delayed fetal pulmonary maturation occurred without fetal hyperinsulinism which suggests that this latter feature may not be of crucial significance in the aetiology of the respiratory distress syndrome.
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PMID:Development of phosphatidyl glycerol biosynthesis in the lungs of fetuses of diabetic rats. 634 Nov 49

Because respiratory distress syndrome (RDS) may occur in one twin but not the other it may be misleading to assess fetal lung maturity using amniotic fluid from only one sac. We compared the amniotic fluid lecithin/sphingomyelin (L/S), phosphatidyl glycerol/sphingomyelin (PG/S) and phosphatidyl inositol/sphingomyelin (PI/S) ratios between co-twins and co-triplets in 32 sets of twins and three set of triplets. In the twin pregnancies we found a weak correlation for L/S ratio but a much improved one for PG/S and PI/S. The concordance between sacs for all three ratios was better in monozygotic than in dizygotic twins. The efficacy of amniotic fluid PG in the determination of fetal lung maturity was demonstrated and the discrepancies between the sacs was much less for PG than for the L/S ratios. Employing the L/S ratio combined with the presence or absence of PG should reduce false results to a minimum.
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PMID:Amniotic fluid phospholipid profile in multiple pregnancy and the effect of zygosity. 663 96

Phosphatidyl-glycerol (PG) and the lecithin/sphingomyelin (L/S) ratio were determined on amniotic fluid from 140 patients to evaluate the role of PG estimation as a functional fetal lung maturity test. PG was absent without associated respiratory distress syndrome (RDS) in 17 cases (12%) and present in 123, 3 of the infants born to these patients developed slight hyaline membrane disease. There were no neonatal deaths. When both PG and the L/S ratio were determined the accuracy of prediction of the RDS improved from 87% to 93%. PG determination should not be used as a substitute for the L/S ratio, but should be used in conjunction with it in high-risk situations.
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PMID:The role of phosphatidyl-glycerol in the determination of fetal lung maturity. 684 62


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