Tsang, Siu Wai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 107-121). / Abstracts in English and Chinese. / Abstract --- p.i / 摘要 --- p.iii / Acknowledgements --- p.v / Table of Contents --- p.vi / List of Abbreviations --- p.x / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- Renin-angiotensin system (RAS) --- p.1 / Chapter 1.1.1 --- Circulating RAS --- p.2 / Chapter 1.1.2 --- Tissue-specific RAS --- p.5 / Chapter 1.2 --- RAS inhibitors --- p.7 / Chapter 1.2.1 --- Angiotensin converting enzyme inhibitor --- p.8 / Chapter 1.2.2 --- Non-specific angiotensin II receptor blocker --- p.9 / Chapter 1.2.3 --- Specific AT1 receptor antagonist --- p.10 / Chapter 1.2.4 --- Specific AT2 receptor antagonist --- p.11 / Chapter 1.3 --- Pancreas and functions of exocrine pancreas --- p.14 / Chapter 1.3.1 --- Structure of pancreas --- p.14 / Chapter 1.3.2 --- Exocrine secretions and pancreatic enzymes --- p.16 / Chapter 1.3.3 --- Regulation of exocrine secretions --- p.17 / Chapter 1.4 --- Pancreatic RAS --- p.18 / Chapter 1.4.1 --- Expression and localization --- p.18 / Chapter 1.4.2 --- Regulation --- p.19 / Chapter 1.4.3 --- Clinical relevance to the pancreas --- p.20 / Chapter 1.5 --- Acute pancreatitis --- p.21 / Chapter 1.5.1 --- Pathogenesis --- p.21 / Chapter 1.5.2 --- Experimental models of acute pancreatitis --- p.22 / Chapter 1.5.3 --- Criteria of acute pancreatitis --- p.23 / Chapter 1.5.4 --- Oxidative stress in acute pancreatitis --- p.24 / Chapter 1.6 --- RAS and acute pancreatitis in exocrine pancreas --- p.26 / Chapter 1.6.1 --- RAS and acute pancreatitis --- p.26 / Chapter 1.6.2 --- RAS and pancreatic microcirculation --- p.26 / Chapter 1.6.3 --- RAS and tissue injury --- p.27 / Chapter 1.6.4 --- Exocrine pancreatic RAS and acute pancreatitis-induced injury --- p.28 / Chapter 1.7 --- Aims of study --- p.29 / Chapter Chapter 2 --- Materials and Methods / Chapter 2.1 --- Animal models and RAS inhibitors --- p.30 / Chapter 2.1.1 --- Cerulein-induced acute pancreatitis --- p.30 / Chapter 2.1.2 --- Prophylactic treatment with RAS inhibitors --- p.31 / Chapter 2.1.3 --- Therapeutic treatment with RAS inhibitors --- p.32 / Chapter 2.2 --- Evaluation of pancreatic injury --- p.32 / Chapter 2.2.1 --- Assessment of pancreatic water content --- p.33 / Chapter 2.2.2 --- Measurement of α-amylase activity in plasma --- p.33 / Chapter 2.2.3 --- Measurement of lipase activity in plasma --- p.34 / Chapter 2.3 --- Histopathological examinations --- p.34 / Chapter 2.3.1 --- Preparation of paraffin blocks --- p.35 / Chapter 2.3.2 --- Hematoxylin and eosin staining --- p.35 / Chapter 2.4 --- Biochemical assay of pancreatic oxidative status --- p.37 / Chapter 2.4.1 --- Sample preparation --- p.37 / Chapter 2.4.2 --- Quantification of protein content --- p.37 / Chapter 2.4.3 --- Measurement of glutathione levels --- p.38 / Chapter 2.4.4 --- Assessment of protein oxidation --- p.38 / Chapter 2.4.5 --- Assessment of lipid peroxidation --- p.39 / Chapter 2.4.6 --- Measurement of NADPH oxidase activity --- p.40 / Chapter 2.5 --- Studies of pancreatic digestive enzyme secretions from isolated acini --- p.40 / Chapter 2.5.1 --- Dissociation of acini from pancreatic tissue --- p.40 / Chapter 2.5.2 --- Treatment with peptides and RAS inhibitors --- p.42 / Chapter 2.5.3 --- Quantification of protein and DNA contents --- p.43 / Chapter 2.5.4 --- Measurement of a-amylase and lipase secretions --- p.44 / Chapter 2.5.5 --- RT-PCR analysis of RAS components in acinar cells --- p.44 / Chapter 2.6 --- Studies of RAS inhibitors on acute pancreatitis-induced systemic inflammation --- p.45 / Chapter 2.6.1 --- Systemic inflammation treatment --- p.45 / Chapter 2.6.2 --- Measurement of myeloperoxidase activity in lung and liver --- p.46 / Chapter 2.7 --- Statistical analysis --- p.47 / Chapter Chapter 3 --- Results / Chapter 3.1 --- Time-course experiment of acute pancreatitis model --- p.48 / Chapter 3.1.1 --- Effect of acute pancreatitis on tissue injury --- p.48 / Chapter 3.1.2 --- Effects of acute pancreatitis on oxidative status --- p.48 / Chapter 3.2 --- Evaluation of ramiprilat and saralasin on changes of acute pancreatitis- induced pancreatic injury --- p.50 / Chapter 3.2.1 --- Changes in tissue injury and histopathology --- p.50 / Chapter 3.2.2 --- Changes in oxidative status --- p.57 / Chapter 3.3 --- Evaluation of losartan and PD123319 on changes of acute pancreatitis- induced pancreatic injury --- p.61 / Chapter 3.3.1 --- Changes in tissue injury and histopathology --- p.61 / Chapter 3.3.2 --- Changes in oxidative status --- p.68 / Chapter 3.4 --- Evaluation of acinar secretions of digestive enzymes --- p.71 / Chapter 3.4.1 --- Cholecystokinin octapeptide-induced acinar secretions --- p.71 / Chapter 3.4.2 --- Angiotensin II-induced acinar secretions --- p.71 / Chapter 3.4.3 --- Effects of losartan and PD 123319 on α-amylase secretion --- p.74 / Chapter 3.5 --- Existence and regulation of acinar RAS by acute pancreatitis --- p.75 / Chapter 3.5.1 --- Expression of angiotensinogen and its regulation by acute pancreatitis in acini --- p.76 / Chapter 3.5.2 --- Expression of AT1 receptor and its regulation by acute pancreatitis in acini --- p.76 / Chapter 3.5.3 --- Expression of AT2 receptor and its regulation by acute pancreatitis in acini --- p.76 / Chapter 3.5.4 --- Evaluation of RAS inhibitors in acute pancreatitis-induced acinar cells --- p.80 / Chapter 3.6 --- Preliminary data on acute pancreatitis-induced systemic inflammation --- p.81 / Chapter 3.6.1 --- Time-course experiment on lung injury --- p.81 / Chapter 3.6.2 --- Time-course experiment on liver injury --- p.83 / Chapter 3.6.3 --- Evaluation of losartan on systemic inflammation --- p.85 / Chapter Chapter 4 --- Discussion / Chapter 4.1 --- "Actions of RAS inhibitors on the changes of tissue injury, oxidative status and histopathology in acute pancreatitis-induced pancreas" --- p.87 / Chapter 4.1.1 --- Differential effects of ramiprilat and saralasin --- p.88 / Chapter 4.1.2 --- Differential effects of losartan and PD123319 --- p.92 / Chapter 4.2 --- Potential functions of RAS in pancreatic acinar secretions --- p.95 / Chapter 4.2.1 --- Potential role of AT1 receptor --- p.96 / Chapter 4.2.2 --- Potential role of AT2 receptor --- p.98 / Chapter 4.3 --- Regulation of RAS in acute pancreatitis-induced acini --- p.98 / Chapter 4.3.1 --- Regulation of RAS components in acinar cells --- p.99 / Chapter 4.3.2 --- Differential actions of losartan and PD123319 --- p.100 / Chapter 4.4 --- Potential role of RAS in acute pancreatitis --- p.102 / Chapter 4.4.1 --- Regulation of RAS components by acute pancreatitis --- p.102 / Chapter 4.4.2 --- Differential functions of AT1 and AT2 receptors in acute pancreatitis --- p.103 / Chapter 4.5 --- Conclusion --- p.104 / Chapter 4.6 --- Further studies --- p.105 / Chapter Chapter 5 --- Bibliography --- p.107
| Identifer | oai:union.ndltd.org:cuhk.edu.hk/oai:cuhk-dr:cuhk_324501 |
| Date | January 2003 |
| Contributors | Tsang, Siu Wai., Chinese University of Hong Kong Graduate School. Division of Physiology. |
| Source Sets | The Chinese University of Hong Kong |
| Language | English, Chinese |
| Detected Language | English |
| Type | Text, bibliography |
| Format | print, x, 121 leaves : ill. ; 30 cm. |
| Rights | Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/) |
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