Thesis (D.Sc.)--University of the Witwatersrand, Faculty of Health Sciences, 2012.

Tse On Ki. / Thesis submitted in: June, 1997. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 97-113). / Abstract also in Chinese. / List of Tables --- p.xiii / List of Figures --- p.xiv / List of Abbreviations --- p.xv / Chapter Chapter 1. --- Introduction to thesis --- p.2 / Chapter 1.1 --- Misoprostol --- p.2 / Chapter 1.1.1 --- Description and History of Drug --- p.2 / Chapter 1.1.2 --- Current Use in Obstetrics and Gynaecology --- p.3 / Chapter 1.1.2.1 --- Termination of Pregnancy (TOP) --- p.3 / Chapter 1.1.2.2 --- Cervix Priming prior to Surgical Treatment of Pregnancy Failure --- p.4 / Chapter 1.1.2.3 --- Medical management of spontaneous abortion --- p.4 / Chapter 1.2 --- Gemeprost --- p.4 / Chapter 1.3 --- Doppler Sonography and Assessment of Blood Velocity --- p.5 / Chapter 1.4 --- Overview of Thesis --- p.5 / Chapter 1.5 --- Aim of this Study --- p.8 / Chapter Chapter 2. --- Physiological and Anatomical Features of Pregnancy --- p.10 / Chapter 2.1 --- Cardiovascular System Changes in Pregnancy --- p.10 / Chapter 2.1.1 --- Changes in the Blood --- p.10 / Chapter 2.1.2 --- Changes in Circulation --- p.11 / Chapter 2.1.3 --- The Distribution of Blood Flow in Uterus --- p.12 / Chapter 2.2 --- Blood Supply to Uterus --- p.13 / Chapter 2.3 --- Pelvic Anatomy in Early Pregnancy via Transvaginal Sonography --- p.15 / Chapter 2.3.1 --- Uterus --- p.15 / Chapter 2.3.2 --- The Adnexa --- p.17 / Chapter 2.3.3 --- Other Pelvic Structures --- p.17 / Chapter Chapter 3. --- Prostaglandins and Analogues --- p.19 / Chapter 3.1 --- Natural Prostaglandins --- p.19 / Chapter 3.2 --- The Source of PGs in Reproductive Organs of Women --- p.19 / Chapter 3.3 --- PGs Synthesis and Metabolism --- p.20 / Chapter 3.4 --- PGE1 Analogue: Misoprostol --- p.21 / Chapter 3.4.1 --- Misoprostol --- p.22 / Chapter 3.4.1.1 --- Pharmacology --- p.22 / Chapter 3.4.1.2 --- Adverse Side Effects --- p.23 / Chapter 3.4.1.3 --- Toxicology --- p.23 / Chapter 3.4.1.4 --- Misoprostol in Obstetrics & Gynaecology --- p.24 / Chapter 3.4.1.4.1 --- To Induce Abortion in First and Second Trimesters --- p.24 / Chapter 3.4.1.4.2 --- Cervix Priming prior to Surgical Evacuation of Uterus --- p.27 / Chapter 3.4.1.4.3 --- Medical Management of Miscarriage --- p.28 / Chapter 3.4.1.4.4 --- Induction of Labour with Dead Fetus --- p.29 / Chapter 3.4.1.4.5 --- Induction of labour --- p.29 / Chapter 3.4.2 --- The Potential Dangers of PGE1 analogues --- p.30 / Chapter Chapter 4. --- Doppler Sonography and Parameter Measurements --- p.34 / Chapter 4.1 --- The Principles of Ultrasound and Doppler Sonography --- p.34 / Chapter 4.1.1 --- The Basic Principles of Ultrasound --- p.34 / Chapter 4.1.2 --- Principles of Doppler Sonography --- p.36 / Chapter 4.2 --- Doppler Mode --- p.39 / Chapter 4.2.1 --- Continuous Wave Doppler Imaging --- p.39 / Chapter 4.2.2 --- Pulsed Wave Doppler Systems --- p.39 / Chapter 4.2.3 --- Colour Doppler Sonography (CDS) --- p.40 / Chapter 4.3 --- The Instrument of Doppler Sonography --- p.40 / Chapter 4.4 --- "Resistance Indices - S/D, PI and RI" --- p.42 / Chapter 4.5 --- Flow Measurement of Uterine artery --- p.44 / Chapter 4.5.1 --- Sampling Sites and Waveforms --- p.44 / Chapter 4.5.2 --- Waveform Components --- p.45 / Chapter 4.5.3 --- Identification of the Main Uterine Arteries --- p.45 / Chapter 4.5.4 --- UA Waveform Changes in Normal Pregnancy --- p.46 / Chapter 4.5.5 --- Factors Affecting the UA Waveforms --- p.48 / Chapter 4.5.6 --- Uterine Artery Resistance in Normal Pregnancy and Labour --- p.49 / Chapter 4.5.6.1 --- Uterine Artery Resistance in Normal Pregnancy --- p.49 / Chapter 4.5.6.2 --- Uterine Artery Resistance during normal labour --- p.51 / Chapter 4.5.7 --- Doppler Measure of Fetal Heart Rate --- p.52 / Chapter 4.6 --- Sonography in Estimation of Gestational Age --- p.53 / Chapter Chapter 5. --- Research Protocol --- p.56 / Chapter 5.1 --- The Ethics --- p.56 / Chapter 5.2 --- Apparatus --- p.58 / Chapter 5.3 --- Drug and Dosage --- p.59 / Chapter 5.4 --- Research Protocol --- p.59 / Chapter 5.4.1 --- Subjects --- p.59 / Chapter 5.4.2 --- Transvaginal Scan --- p.60 / Chapter 5.4.3 --- Parameters Measured --- p.61 / Chapter 5.4.4 --- Misoprostol --- p.65 / Chapter 5.5 --- Data analysis --- p.66 / Chapter Chapter 6. --- Results --- p.68 / Chapter 6.1 --- The Patients' Characteristics --- p.68 / Chapter 6.2 --- The Intra-observer Error --- p.70 / Chapter 6.3 --- Results of Study --- p.70 / Chapter 6.3.1 --- Effect of Misoprostol on the S/D ratio of Both Uterine Arteries --- p.70 / Chapter 6.3.2 --- Effect of Misoprostol on the PI of Both Uterine Arteries --- p.73 / Chapter 6.3.3 --- Effect of Misoprostol on Fetal Heart Rate (FHR) --- p.76 / Chapter 6.3.4 --- Left and Right UA-S/D --- p.78 / Chapter 6.3.5 --- Left and Right UA-PI --- p.81 / Chapter 6.3.6 --- The relationship Between Subgroups --- p.84 / Chapter 6.3.7 --- Side Effects of Misoprostol --- p.85 / Chapter 6.3.8 --- The Changes of UA-S/D and UA-PI According to Gestation --- p.86 / Chapter Chapter 7. --- Discussions and Conclusions --- p.89 / Chapter 7.1 --- Difficulties Encountered during Study --- p.89 / Chapter 7.2 --- Results of Study --- p.90 / Chapter 7.3 --- Implications --- p.94 / Chapter 7.4 --- Summary of Thesis --- p.95 / Chapter 7.5 --- Conclusions --- p.96 / Chapter 8. --- References and Appendix --- p.97

Sucralfate is a drug that effectively heals duodenal, gastric and oesophageal ulcers. It is not absorbed systemically and it has been shown to act locally by coating the ulcer base. However when it was also shown to prevent stress ulcers and ethanolinduced gastric mucosa! lesions, it seemed likely that it acted in some way to improve the effectiveness of the gastric mucosa! barrier. Some investigators suggested that it did so by stimulating local prostaglandin release. The Slomiany group, on the basis of in vitro work on the effects of Sucralfate on pig gastric mucus, claimed that Sucralfate acted by altering the physico-chemical properties of mucus to increase the viscosity and retard the back diffusion of H+ ions. The work described in this dissertation set out to verify, in vivo, these claimed effects on mucus, using an experimental porcine model of peptic ulceration, the bile duct ligated pig. In addition, the effects of Sucralfate were compared with those of Famotidine and Misoprostol, and changes in mucous prostaglandins, gastric juice pepsin and gastric flora were sought. By way of introduction, the known and postulated actions of Sucralfate, current understanding of gastric mucus physiology and pathogenesis of peptic ulceration, have been reviewed, as have experimental animal models of peptic ulceration, in order to justify using the bile duct ligated pig model.