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Liu Bao Yi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (leaves 83-104). / Abstracts in English and Chinese. / ABSTRACT --- p.i / ACKNOWLEDGEMENT --- p.v / TABLE OF CONTENTS --- p.vi / LIST OF ABBREVIATIONS --- p.xii / LIST OF FIGURES --- p.xivv / LIST OF TABLES --- p.xv / PUBLICATION RELATED TO THIS THESIS --- p.xvii / Chapter PART 1 --- INTRODUCTION AND LITERATURE RESEARCH / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter CHAPTER 2 --- MECONIUM STAINED LIQUOR --- p.3 / Chapter 2.1 --- AMNIOTIC FLUID --- p.3 / Chapter 2.1.1 --- Function of Amniotic Fluid --- p.3 / Chapter 2.1.2 --- Composition Of Amniotic Fluid --- p.3 / Chapter 2.1.3 --- Regulation Of Amniotic Fluid --- p.4 / Chapter 2.1.4 --- Abnormality Of Amniotic Fluid Volume --- p.4 / Chapter 2.2 --- MECONIUM STAINED LIQUOR --- p.6 / Chapter 2.2.1 --- Formation And Composition Of Meconium --- p.6 / Chapter 2.2.2 --- Peristalsis Of Fetal Gastrointestinal Tract --- p.7 / Chapter 2.2.3 --- Meconium Stained Liquor(MSL) --- p.7 / Chapter 2.2.3.1 --- Maturation Theory --- p.7 / Chapter 2.2.3.2 --- Cord Compression Theory --- p.9 / Chapter 2.2.3.3 --- Fetal Hypoxia Theory --- p.10 / Chapter 2.2.4 --- Fetal Effect Of Meconium In Amniotic Cavity --- p.11 / Chapter 2.2.5 --- Meconium Aspiration Syndrome --- p.12 / Chapter 2.2.6 --- Clinical Significance And Limitation Of Studies --- p.13 / Chapter 2.3 --- Purpose Of Study --- p.14 / Chapter CHAPTER 3 --- OXIDATIVE STRESS AND FETAL HYPOXIA --- p.16 / Chapter 3.1 --- OXIDATIVE STRESS --- p.16 / Chapter 3.2 --- FREE RADICALS --- p.16 / Chapter 3.2.1 --- Sources Of Free Radicals --- p.17 / Chapter 3.2.1.1 --- Biological Source Of Free Radicals --- p.17 / Chapter 3.2.1.2 --- Intracellular Source Of Free Radicals --- p.17 / Chapter 3.2.1.3 --- Composition Of Free Radicals And Reactive Oxygen Species --- p.18 / Chapter 3.2.2 --- Cellular Components At Risk From Free Radicals Damage --- p.20 / Chapter 3.2.2.1 --- Proteins --- p.20 / Chapter 3.2.2.2 --- Nucleic Acids And DNA --- p.21 / Chapter 3.2.2.3 --- Membrane Lipids --- p.21 / Chapter 3.2.3 --- Lipid Peroxidation --- p.21 / Chapter 3.2.3.1 --- Chemical Substances Of Membranes --- p.21 / Chapter 3.2.3.2 --- The Reactions Of Lipid Peroxidation --- p.22 / Chapter 3.2.3.3 --- Lipid Peroxidation In Pregnancy --- p.23 / Chapter 3.2.4 --- Protection Against Lipid Peroxidation --- p.24 / Chapter 3.2.5 --- Isoprostanes --- p.26 / Chapter 3.2.5.1 --- Definition --- p.26 / Chapter 3.2.5.2 --- Formation Of Isoprostanes --- p.26 / Chapter 3.2.5.3 --- Metabolism Of Isoprostanes --- p.27 / Chapter 3.2.5.4 --- Biological Characteristics Of Isoprostanes --- p.29 / Chapter 3.2.5.5 --- Isoprostanes As Mediators Of Oxidantive Stress --- p.29 / Chapter 3.3 --- FETAL HYPOXIA --- p.30 / Chapter 3.3.1 --- Fetal Metabolism And Energy Supply --- p.30 / Chapter 3.3.2 --- Free Radical Generation And Fetal Hypoxia-Reoxygenation --- p.33 / Chapter 3.3.3 --- Fetal Hypoxia And Fetal Brain Injury --- p.34 / Chapter 3.3.4 --- Measurement Of Fetal Hypoxia --- p.35 / Chapter 3.3.4.1 --- Acid-Base Balance --- p.35 / Chapter 3.3.4.2 --- Fetal Heart Rate Monitoring --- p.36 / Chapter 3.3.4.3 --- Apgar scores --- p.37 / Chapter 3.3.4.4 --- Pulse Oximetry --- p.37 / Chapter 3.3.4.5 --- Lipid Peroxides --- p.38 / Chapter CHAPTER 4 --- AMNIOINFUSION --- p.40 / Chapter 4.1 --- AMNIOINFUSION --- p.40 / Chapter 4.2 --- AMNIOINFUSION FOR OLIGOHYDRAMNIOS --- p.40 / Chapter 4.3 --- AMNIOINFUSION FOR MECONIUM STAINED LIQUOR --- p.41 / Chapter 4.4 --- PURPOSE OF THE STUDY --- p.42 / Chapter PART 2 --- CLINICAL PROTOCOLS AND MEASUREMENT OF ISOPROSTANES / Chapter CHAPTER 5 --- CLINICAL PROTOCOLS --- p.43 / Chapter 5.1 --- ETHICS --- p.43 / Chapter 5.2 --- CLINICAL PROTOCOLS --- p.43 / Chapter 5.2.1 --- Artificial Rupture Of Membranes (Amniotomy) --- p.43 / Chapter 5.2.2 --- Classification of Meconium Stained Liquor --- p.44 / Chapter 5.2.3 --- Electronic Fetal Heart Rate Monitoring --- p.44 / Chapter 5.2.4 --- Monitoring The Progress of Labour --- p.44 / Chapter 5.2.5 --- Umbilical Cord Blood Gas Analysis --- p.45 / Chapter 5.2.6 --- Apgar Score --- p.45 / Chapter 5.2.7 --- Meconium Aspiration --- p.46 / Chapter 5.2.8 --- Clinical Outcome --- p.46 / Chapter CHAPTER 6 --- MEASUREMENT OF ISOPROSTANES --- p.50 / Chapter 6.1 --- BLOOD PREPARATION --- p.50 / Chapter 6.2 --- REAGENTS --- p.50 / Chapter 6.3 --- GAS CHROMATOGRAPHY AND MASS SPECTROMETRY (GC-MS) --- p.51 / Chapter 6.4 --- PROCEDURES --- p.51 / Chapter 6.5 --- DATA RELIABILITY --- p.53 / Chapter PART 3 --- RESULTS AND DISCUSSION / Chapter CHAPTER 7 --- MECONIUM STAINED LIQUOR (MSL) DURING LABOUR AND NEONATAL CORD BLOOD 8-IS〇-PGF2α CONCENTRATION --- p.54 / Chapter 7.1 --- OBJECTIVE --- p.54 / Chapter 7.2 --- MATERIALS AND METHOD --- p.55 / Chapter 7.3 --- STATISTICAL ANALYSIS --- p.56 / Chapter 7.4 --- RESULTS --- p.57 / Chapter 7.5 --- DISCUSSION --- p.65 / Chapter 7.6 --- CONCLUSION --- p.67 / Chapter CHAPTER 8 --- EVALUATION OF PROPHYLACTIC AMNIOINFUSION FOR INTRAPARTUM MECONIUM STAINED LIQUOR --- p.69 / Chapter 8.1 --- OBJECTIVE --- p.69 / Chapter 8.2 --- MATERIALS AND METHOD --- p.69 / Chapter 8.2.1 --- Study Group: 226}0ب MSL+AI' --- p.69 / Chapter 8.2.2 --- The Procedure Of Amnioinfusion --- p.70 / Chapter 8.2.3 --- Other Study Group --- p.71 / Chapter 8.3 --- STATISTIC ANALYSIS --- p.71 / Chapter 8.4 --- RESULTS --- p.72 / Chapter 8.4.1 --- Comparison Between The 'MSL+AI' And 'MSL-AI' Groups --- p.72 / Chapter 8.4.2 --- Comparison Between 226}0بMSL+AI'And 'Clear Liquor' Groups --- p.74 / Chapter 8.5 --- DISCUSSION --- p.77 / Chapter 8.6 --- CONCLUSION --- p.79 / Chapter CHAPTER 9 --- COMMENTS AND FUTURE RESEARCH --- p.80 / BIBLIOGRAPHY --- p.83

The study objectives were to: (1) assess fetal exposure to oxidative stress by measuring amniotic fluid concentrations of nitric oxide (NO), thiobarbituric acid--reactive substances (TBARS), and ferric reducing antioxidant power (FRAP) and (2) establish whether these concentrations were associated with infant birth weight, gestational age, or oxidative stress-related conditions arising during pregnancy. Frozen amniotic fluid samples were obtained from 654 mothers undergoing amniocentesis for genetic testing during second trimester in Montreal, QC, Canada. Maternal and neonatal characteristics were collected from medical charts and questionnaires and exclusion criteria were applied. ANOVAs and multivariate regression analyses showed that NO, which differed among pre-term, term, and post-term groups, was a positive predictor of gestational age. TBARS were highly correlated with sample storage and were not associated with pregnancy outcome parameters. FRAP positively predicted gender-corrected birth-weight-for-gestational-age. Our study shows that markers of oxidative and nitrative stress in-utero are associated with pregnancy outcomes.

The study objective was to determine whether early 2 nd trimester amniotic fluid (AF) erythropoietin (EPO) was associated with and predictive of (a) development of maternal gestational diabetes (GDM) and (b) the infant outcome parameters of (i) gestational age at birth (GAAB) assessed exclusively among spontaneous vaginal deliveries or (ii) birth weight (measured in grams and percentiles). Enzyme-linked-immunosorbent assay was used to determine the EPO concentration of 170 biobanked AF samples. Student's t-test revealed no difference between GDM and non-GDM subjects. AF EPO was not predictive of GAAB despite being significantly greater among preterm infants compared to post-term infants. In contrast, AF EPO was significantly higher among the smallest infants using both birth weight classification schemes. However, following inclusion of known covariates AF EPO was predictive of gram birth weight only. Early 2nd trimester AF EPO may emerge as a useful biomarker of fetal nutritional status and/or growth.

The objectives were (1) to establish a profile of total fatty acids and cholesterol in amniotic fluid (AF) as well as (2) to determine possible associations between AT fatty acids (micromolar and relative proportion) with gestational age and birth weight. A total of 208 AF samples collected between 12 and 22 weeks of gestation during routine amniocentesis were analyzed using tandem column gas chromatography (GC). Smoking increased AF polyunsaturated fatty acid (PUFAs) levels while developmental stage and storage time decreased AF fatty acid quantities. AF trans fatty acids (TFAs) were negatively associated with both birth outcomes, whereas specific fatty acids including stearic acid (C18:0) and gondoic acid (C20:1n-9) were identified as negative predictors for gestational age and birth weight respectively. This study demonstrated novel relationships between fatty acids and fetal growth and gestational age in early midgestation AF, suggesting a possible role of AF fatty acids in predicting birth outcomes.

This study was designed to examine the hypothesis that the amount of amniotic fluid present during gestation is critical to normal lung growth and maturation. On day 16 of gestation the amniotic sacs of the right or left uterine horns of timed pregnant Sprague-Dawley rats were punctured with a 20 gauge needle. The fetuses of the opposite horn served as controls. On day 21 of gestation (one day prior to natural delivery) the fetuses were delivered by Cesarean section. An unbalanced, mixed model analysis of variance was performed on the data collected from each fetus. Probability values of less than 0.05 between control and experimental animals were considered significant. Amniotic sac puncture resulted in a significant loss of amniotic fluid as indicated by reduced amniotic fluid volume on day 21. Experimental body weight was significantly reduced indicating fetal growth retardation. Lung growth was also retarded as indicated by significantly reduced lung weight to body weight ratios and lung volume to body weight ratios following amniotic sac puncture. There was a reduction in the amount of fluid present within the experimental lungs. There appeared to be no significant effect on the structural units of the lung as indicated by no significant difference between control and experimental fetal lungs in terms of cell number, cell size, total protein to body weight ratio, maturation of type II cells, volume fraction of saccular air, saccular wall, conducting air and nonparenchyma, airspace size, saccular surface area to body weight ratio and surface to volume ratio. Thus, loss of amniotic fluid significantly affected lung growth, more than it affected overall body growth, without having an effect on lung maturation. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate

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