Cheung Ho Yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 164-175). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgements --- p.vi / Publications based on the work in this thesis --- p.vii / Table of content --- p.viii / Abbreviations --- p.xii / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Traditional Chinese Medicine --- p.1 / Chapter 1.1.1 --- Danshen --- p.2 / Chapter 1.1.2 --- Chemical constituents --- p.5 / Chapter 1.1.3 --- Pharmacological effects --- p.7 / Chapter 1.1.3.1 --- On blood vessels --- p.7 / Chapter 1.1.3.2 --- On blood pressure --- p.8 / Chapter 1.1.3.3 --- On heart --- p.8 / Chapter 1.1.3.4 --- On myocardial ischaemia and reperfusion --- p.9 / Chapter 1.1.3.5 --- On platelet activity --- p.10 / Chapter 1.1.3.6 --- Other actions --- p.11 / Chapter 1.1.4 --- Clinical studies --- p.12 / Chapter 1.2 --- The Vascular System --- p.13 / Chapter 1.2.1 --- The circulation network --- p.13 / Chapter 1.2.2 --- Physiology of blood vessels --- p.13 / Chapter 1.2.3 --- Control of vascular lone --- p.14 / Chapter 1.3 --- Mechanisms of Vasodilatation --- p.16 / Chapter 1.3.1 --- Endothelium derived relaxant factors (EDRFs) --- p.16 / Chapter 1.3.1.1 --- Nitric oxide (NO) --- p.16 / Chapter 1.3.1.2 --- Prostacyclin (PGI：) --- p.17 / Chapter 1.3.1.3 --- Endotheliun-derived hyperpolarization factors (EDHFs) --- p.18 / Chapter 1.3.1.3.1 --- Epoxyeicosatrienoic acids (EETs) --- p.19 / Chapter 1.3.1.3.2 --- Potassium ion (IC) --- p.20 / Chapter 1.3.1.3.3 --- Gap junction --- p.20 / Chapter 1.3.2 --- Signal transduction pathways --- p.21 / Chapter 1.3.2.1 --- Guanylyl cyclase-cGMP pathway --- p.21 / Chapter 1.3.2.2 --- Adenylyl cyclase-cAMP pathway --- p.22 / Chapter 1.3.3 --- Ion channels in vascular smooth muscle cell --- p.24 / Chapter 1.3.3.1 --- Potassium channels (K+ channels) --- p.24 / Chapter 1.3.3.2 --- Calcium channels (Ca2+ channels) --- p.24 / Chapter 1.3.3.3 --- Chloride channel (Cl channel) --- p.25 / Chapter 1.3.4 --- Receptor-operated mechanisms --- p.27 / Chapter 1.3.4.1 --- Muscarinic receptors --- p.27 / Chapter 1.3.4.2 --- Adrenoceptors --- p.27 / Chapter 1.3.4.3 --- Histamine receptors --- p.28 / Chapter 1.3.4.4 --- CGRP receptors --- p.29 / Chapter 1.3.4.5 --- Tachykinin receptors --- p.30 / Chapter 1.4 --- Aims of the studies --- p.31 / Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.32 / Chapter 2.1 --- Extraction of Water and Lipid-solubie Fractions from Danshen --- p.32 / Chapter 2.1.1 --- Preparation of water-soluble and lipid-soluble fractions --- p.33 / Chapter 2.2 --- Experiments on Rat Knee Joint --- p.35 / Chapter 2.2.1 --- Animals --- p.35 / Chapter 2.2.2 --- Materials --- p.35 / Chapter 2.2.3 --- Preparatory protocols --- p.37 / Chapter 2.2.3.1 --- Anaesthesia of animals --- p.37 / Chapter 2.2.3.2 --- Cannulation of trachea --- p.37 / Chapter 2.2.3.3 --- Cannulation of carotid artery --- p.38 / Chapter 2.2.3.4 --- Blood pressure measurement --- p.38 / Chapter 2.2.4 --- Measurement of knee joint blood flow --- p.39 / Chapter 2.2.4.1 --- Preparation for measurement of knee joint blood flow --- p.41 / Chapter 2.2.5 --- Experimental protocols --- p.41 / Chapter 2.2.5.1 --- Danshen on knee joint blood flow --- p.41 / Chapter 2.2.5.2 --- Antagonists on Danshen --- p.41 / Chapter 2.2.5.3 --- Positive controls --- p.43 / Chapter 2.2.6 --- Image analysis --- p.44 / Chapter 2.2.7 --- Data analysis --- p.44 / Chapter 2.3 --- Experiments on Rat Femoral Artery --- p.45 / Chapter 2.3.1 --- Animals --- p.45 / Chapter 2.3.2 --- Materials --- p.45 / Chapter 2.3.2.1 --- Chemicals --- p.45 / Chapter 2.3.2.2 --- Physiological salt solution --- p.48 / Chapter 2.3.3 --- Preparatory protocols --- p.48 / Chapter 2.3.3.1 --- Small vessel myograph --- p.48 / Chapter 2.3.3.2 --- Isolation and mounting of tissue --- p.49 / Chapter 2.3.4 --- Experimental protocols --- p.50 / Chapter 2.3.4.1 --- Studies on the vasodilator response to Danshen --- p.50 / Chapter 2.3.4.2 --- Studies of antagonists on Danshen --- p.50 / Chapter 2.3.4.2.1 --- Endothelium-dependent mechanisms --- p.51 / Chapter 2.3.4.2.2 --- Endothelium-independent mechanisms --- p.54 / Chapter 2.3.4.2.3 --- K+ channel blockers --- p.54 / Chapter 2.3.4.2.4 --- Positive controls --- p.55 / Chapter 2.3.4.3 --- Danshen on Ca2+-induced contraction --- p.56 / Chapter 2.3.5 --- Data analysis --- p.57 / Chapter CHAPTER 3 --- RESULTS --- p.58 / Chapter 3.1 --- Danshen on Rat Knee Joint Blood Flow --- p.58 / Chapter 3.1.1 --- Topical administration of Danshen --- p.58 / Chapter 3.1.2 --- Antagonists on Danshen --- p.59 / Chapter 3.1.2.1 --- Muscarinic receptor antagonist --- p.59 / Chapter 3.1.2.2 --- β-adrenoceptor antagonist --- p.60 / Chapter 3.1.2.3 --- Histamine receptor antagonists --- p.60 / Chapter 3.1.2.4 --- Nitric oxide synthase inhibitor --- p.61 / Chapter 3.1.2.5 --- Cyclo-oxygenase inhibitors --- p.62 / Chapter 3.1.2.6 --- CGRPi receptor antagonist --- p.62 / Chapter 3.1.2.7 --- NK1 receptor antagonist --- p.63 / Chapter 3.1.2.8 --- Potassium channel inhibitor --- p.64 / Chapter 3.1.2.9 --- "Combination of cyclo-oxygenase inhibitor, nitric oxide synthase inhibitor and CGRP1 receptor antagonist" --- p.64 / Chapter 3.1.3 --- Antagonists on water-soluble fraction of Danshen --- p.91 / Chapter 3.1.3.1 --- Nitric oxide synthase inhibitor --- p.91 / Chapter 3.1.3.2 --- Cyclo-oxygenase inhibitors --- p.91 / Chapter 3.1.3.3 --- CGRP1 receptor antagonist --- p.92 / Chapter 3.1.3.4 --- NK1 receptor antagonist --- p.92 / Chapter 3.1.3.5 --- Potassium channel inhibitor --- p.92 / Chapter 3.2 --- Danshen on Rat Femoral Artery --- p.99 / Chapter 3.2.1 --- Danshen on precontracted arterial ring --- p.99 / Chapter 3.2.2 --- Endothelium-dependent mechanisms --- p.106 / Chapter 3.2.3 --- Endothelium-independent mechanisms --- p.114 / Chapter 3.2.4 --- K+ channel blockers --- p.119 / Chapter 3.2.4.1 --- Effect on Danshen --- p.119 / Chapter 3.2.4.2 --- Effect on water-soluble and lipid-soluble fractions of Danshen --- p.121 / Chapter 3.2.4.3 --- Effect on Danshensu --- p.122 / Chapter 3.2.5 --- Danshen on Ca2+-induced contractions --- p.133 / Chapter CHAPTER 4 --- DISCUSSION --- p.138 / Chapter 4.1 --- In Vivo Studies of Danshen on Rat Knee Joint Blood Flow --- p.139 / Chapter 4.2 --- In Vitro Studies of Danshen on Isolated Rat Femoral Artery --- p.148 / Chapter 4.2.1 --- Comparisons of the use of different precontractors --- p.148 / Chapter 4.2.2 --- Investigations on endothelium-dependent mechanisms --- p.151 / Chapter 4.2.3 --- Investigations on endothelium-independent mechanisms --- p.152 / Chapter 4.2.4 --- Effects of K+ channel blockers --- p.154 / Chapter 4.2.5 --- Inhibition of Ca2+ influx in vascular smooth muscle --- p.157 / Chapter 4.3 --- Comparisons of Results from In Vivo and In Vitro Studies --- p.159 / Chapter 4.4 --- Future Studies --- p.161 / Chapter 4.5 --- Conclusion --- p.162 / REFERENCES --- p.164

Background. Diabetes mellitus is a complex metabolic disorder characterized by clustering of multiple cardiovascular risk factors. Diabetic albuminuria is associated with increased prevalence of both micro-vascular and macro-vascular complications. This thesis examined vascular function (Flow-mediated dilatation, FMD) in type 2 diabetic patients with particular emphasis on its relationships with nephropathy. Independent predictors for FMD in Chinese population using data from both diabetic and non-diabetic subjects as well as the predictive value of FMD on clinical endpoints and death in type 2 diabetic patients with nephropathy were examined. / Conclusions. In Chinese subjects with or without type 2 diabetes, hyperglycaemia, hypertriglyceridemia, smoking and albuminuria were independent predictors for FMD. Type 2 diabetic subjects with overt nephropathy had impaired endothelium-dependent and endothelium-independent dilatation, suggesting vascular dysfunction beyond the endothelium. In agreement with studies from Caucasians, smoking was the most important determinant for vascular dysfunction in Chinese type 2 diabetic patients with overt nephropathy. Furthermore, FMD was predictive of new onset of cardiovascular events and related death in Chinese type 2 diabetic patients with overt nephropathy. / In diabetic patients with overt nephropathy, smoking (current and ex-smokers), waist hip ratio (WHR) and serum creatinine were independent predictors for impaired FMD. The latter was predictive of advancement of IMT and was an independent predictor for new onset of combined cardiovascular diseases and related death after a follow up period of 42 months (log rank test=6.04, p=0.014 using Cox regression analysis) after controlling for all confounding factors. In addition, fasting total cholesterol and plasma glucose were predictive for all-cause mortality while serum creatinine predicted new onset of renal endpoint. In a subgroup analysis in diabetic patients with overt nephropathy, smokers who developed CVD or ESRD had greater diminution of FMD than those who did not develop clinical endpoints. / Methods and results. FMD was assessed using high-resolution ultrasound scan. In the cross-sectional study, the sample population was divided into four groups according to the presence or absence of type 2 diabetes and level of albuminuria. They included the non-diabetic group (N=52), diabetic group with normoalbuminuria (N=18), diabetic group with microalbuminuria (N=18) and diabetic group with overt nephropathy defined as macroalbuminuria and renal insufficiency (N=22). Compared to non-diabetic subjects, type 2 diabetic subjects with nephropathy had impaired FMD (4.54% +/- 2.25 vs. 2.50% +/- 2.31, p<0.05) and impaired GTN-dependent dilatation (GTND) (14.30% +/- 3.77 vs. 12.70% +/- 4.70, p<0.05). They also had reduced endothelium-dependent dilatation to endothelium-independent dilatation ratio when compared to non-diabetic subjects (0.19 +/- 0.17 vs. 0.32 +/- 0.15, p<0.05). These findings suggest that the impaired vascular dilatation was due to dysfunction of both endothelium and vascular smooth muscle cells. In the entire cohort, fasting plasma glucose, fasting triglyceride, smoking and albuminuria were independent predictors for FMD. / Lai Wai Keung Christopher. / "February 2006." / Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6298. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. 202-252). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

Ho, Kwok Wa. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 60-65). / Abstracts in English and Chinese. / Chapter Chapter I / Chapter 1.1. --- Thromboxane A2 (TP) Receptors --- p.1 / Chapter 1.1.1. --- Gene structure of human TP receptors --- p.1 / Chapter 1.1.2. --- Isoforms of TP receptor --- p.1 / Chapter 1.1.3. --- Distribution and expression of TP receptors in human --- p.2 / Chapter 1.1.4. --- Signal transduction of TP receptors --- p.4 / Chapter 1.1.5. --- Major agonists of TP receptor in animals and humans --- p.7 / Chapter 1.1.5.1. --- Thromboxane A2 --- p.7 / Chapter 1.1.5.2. --- Prostaglandin H2 --- p.7 / Chapter 1.1.6. --- Functional studies: effect of TP receptor activation and blockade on vascular tone and atherosclerosis --- p.8 / Chapter 1.1.6.1. --- Effect of TP receptor activation --- p.8 / Chapter 1.1.6.1.1. --- On vaso-contraction --- p.8 / Chapter 1.1.6.1.2. --- On vaso-relaxation --- p.9 / Chapter 1.1.6.2. --- Effect of TP receptor blockade --- p.9 / Chapter 1.1.6.2.1. --- On endothelium dependent vaso-contraction --- p.9 / Chapter 1.1.6.2.2. --- On animal models related to atherosclerosis --- p.10 / Chapter 1.1.7. --- Objectives of current study --- p.10 / Chapter 1.2. --- Periadventitial Adipose (Fat) Tissue --- p.12 / Chapter 1.2.1. --- "General function, distribution and classification of fat" --- p.12 / Chapter 1.2.2. --- Representative endocrine/paracrine role of adipose tissues --- p.13 / Chapter 1.2.2.1. --- Leptin --- p.13 / Chapter 1.2.2.2. --- Angiotensinogen --- p.14 / Chapter 1.2.3. --- Functional studies on vessels with periadventital fat attached -The beginning of the story of adipcyte-derived relaxing factor (ADRF) --- p.15 / Chapter 1.2.3. --- Mechanisms behind the action of ADRF --- p.17 / Chapter 1.2.3.1. --- Nature of ADRF --- p.17 / Chapter 1.2.3.2. --- The mechanisms controlling the release of ADRF --- p.17 / Chapter 1.2.3.3. --- Proposed mechanisms explaining the anti-contractile effect mediated by ADRF --- p.17 / Chapter 1.2.4. --- Objectives of current study --- p.20 / Chapter Chapter II / Chapter 2.1. --- Tissue Preparation --- p.21 / Chapter 2.1.1. --- Preparation of blood vessels --- p.21 / Chapter 2.1.2. --- Procedures to remove the endothelium --- p.21 / Chapter 2.2. --- The Organ Bath Setups --- p.22 / Chapter 2.3. --- Calculation of Results --- p.24 / Chapter 2.3.1. --- Calculation of active tension --- p.24 / Chapter 2.3.2. --- Measurement of dry weight of arterial rings --- p.24 / Chapter 2.3.3. --- Measurement of the weight for periadventitial fat --- p.24 / Chapter 2.3.4. --- Statistic analysis --- p.24 / Chapter 2.4. --- Chemicals and Solutions --- p.25 / Chapter 2.4.1. --- Chemicals --- p.25 / Chapter 2.4.2. --- Solutions --- p.26 / Chapter Chapter III --- Stimulation of TP receptors by U46619 inhibits cGMP dependent vaso-relaxation --- p.27 / Chapter 3.1. --- Detail methods and materials --- p.27 / Chapter 3.1.1. --- "Safety announcement, tissue preparation and materials" --- p.27 / Chapter 3.1.1. --- Protocol --- p.27 / Chapter 3.1.1.1. --- PartI --- p.27 / Chapter 3.1.1.2. --- Part II --- p.28 / Chapter 3.1.1.3. --- Part III --- p.28 / Chapter 3.2. --- Results --- p.29 / Chapter 3.2.1. --- Effect of U46619 on vaso-relaxation --- p.29 / Chapter 3.2.2. --- Effect of Rho kinase and phosphodiesterase inhibitor on the inhibitory effect of U46619 --- p.29 / Chapter 3.2.3. --- The effect of low concentration of U46619 on vaso-relaxation --- p.29 / Chapter 3.3. --- Discussion --- p.37 / Chapter 3.3.1. --- Implication of the current study --- p.37 / Chapter 3.3.2. --- Formulated Theory --- p.41 / Chapter Chapter IV --- Effect of periadventitial fat on anti-relaxation effect induced by U46619 - A preliminary test --- p.43 / Chapter 4.1. --- Detail methods and materials --- p.43 / Chapter 4.1.1. --- "Safety announcement, tissue preparation and materials" --- p.43 / Chapter 4.1.2. --- Protocol --- p.43 / Chapter 4.1.2.1. --- Part I --- p.43 / Chapter 4.1.2.2. --- Part II --- p.44 / Chapter 4.1.2.3. --- Part III --- p.44 / Chapter 4.1.2.4. --- Part IV --- p.44 / Chapter 4.2. --- Results --- p.45 / Chapter 4.2.1. --- Effect of periadventitial fat on vaso-relaxation of rings contracted by phenylephrine --- p.45 / Chapter 4.2.2. --- Effect of periadventitial fat on vaso-relaxation of rings contracted by U46619 plus phenylephrine --- p.45 / Chapter 4.2.3. --- Effect of S18886 on vaso-relaxation in endothelium removed rings --- p.45 / Chapter 4.2.4. --- Effect of elevated extracellular potassium ions on vaso-relaxation --- p.46 / Chapter 4.3. --- Discussion --- p.56 / Chapter 4.3.1. --- Implication of current study --- p.56 / Chapter 4.3.2. --- Improvements and future perspectives of current study --- p.58 / Summary --- p.59 / References --- p.60

Ng Chi Ho. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 147-160). / Abstracts in English and Chinese. / ACKNOWLEDGMENTS --- p.I / ABSTRACT --- p.II / LIST OF ABBREVIATIONS --- p.VII / TABLE OF CONTENTS --- p.IX / Chapter CHAPTER 1 --- GENERAL INTRODUCTION / Chapter 1.1 --- Introduction of Low-density lipoprotein --- p.1 / Chapter 1.1.1 --- What are lipids? --- p.1 / Chapter 1.1.2 --- Function and structure of cholesterol --- p.1 / Chapter 1.1.3 --- Function and classification of lipoprotein --- p.1 / Chapter 1.2 --- Functions of low-density lipoprotein --- p.2 / Chapter 1.3 --- Basic structure of low-density lipoprotein --- p.4 / Chapter 1.4 --- Principle on isolation and purification of low-density lipoprotein --- p.4 / Chapter 1.5 --- Cholesterol transport system --- p.7 / Chapter 1.5.1 --- Exogenous pathway of cholesterol metabolism --- p.7 / Chapter 1.5.2 --- Endogenous pathway of cholesterol metabolism --- p.7 / Chapter 1.5.3 --- Reverse transport of Cholesterol --- p.8 / Chapter 1.6 --- Oxidation of LDL --- p.10 / Chapter 1.6.1 --- Agents that causes oxidation --- p.10 / Chapter 1.6.1.1 --- Lipoxygenases --- p.10 / Chapter 1.6.1.2 --- Myeloperoxidase --- p.10 / Chapter 1.6.1.3 --- Reactive nitrogen species --- p.11 / Chapter 1.6.1.4 --- Reactive oxygen species --- p.11 / Chapter 1.6.2 --- Factors that affect the susceptibility of LDL oxidation --- p.13 / Chapter 1.7 --- Hyperlipidaemia 一 chance to increase LDL oxidation --- p.13 / Chapter 1.7.1 --- Definition of hyperlipidemia and hypercholesterolemia --- p.13 / Chapter 1.7.2 --- Risk factors of hyperlipidaemia --- p.13 / Chapter 1.7.2.1 --- High fat low fibre diets: --- p.13 / Chapter 1.7.2.2 --- Obesity --- p.14 / Chapter 1.7.2.3 --- Type II diabetes --- p.14 / Chapter 1.7.2.4 --- Genetic factors (Familial hyperlipidemias) --- p.14 / Chapter 1.8 --- Diseases related to oxidized LDL --- p.15 / Chapter 1.8.1 --- Cardiovascular diseases --- p.15 / Chapter 1.8.1.1 --- Atherosclerosis and ischemic heart attack --- p.15 / Chapter 1.8.1.2 --- Factors that affect incidence of atherosclerosis --- p.16 / Chapter 1.8.1.2.1 --- Triglyceride-rich lipoprotein --- p.16 / Chapter 1.8.1.2.2 --- Small and dense LDL --- p.16 / Chapter 1.8.1.3 --- Stroke --- p.17 / Chapter 1.8.2 --- Common ways to reduce plasma cholesterol level --- p.17 / Chapter 1.8.2.1 --- Diet control --- p.17 / Chapter 1.8.2.2 --- Physical activity --- p.17 / Chapter 1.8.2.3 --- Drug therapy --- p.18 / Chapter CHAPTER 2 --- IMPAIRMENT OF OXIDIZED LDL ON ENDOTHELIUM-DEPENDENT RELAXATION / Chapter 2.1 --- Introduction --- p.19 / Chapter 2.1.1 --- Properties and function of phenylephrine hydrochloride --- p.22 / Chapter 2.1.2 --- Properties and function of acetylcholine --- p.22 / Chapter 2.2 --- Objectives --- p.23 / Chapter 2.3 --- Materials and methods --- p.24 / Chapter 2.3.1 --- Preparation of drugs --- p.24 / Chapter 2.3.2 --- Preparation of human native LDL --- p.25 / Chapter 2.3.3 --- Preparation of oxidized LDL --- p.27 / Chapter 2.3.4 --- Preparation of aorta --- p.27 / Chapter 2.3.5 --- Measurement of Isometric Force in vitro --- p.30 / Chapter 2.3.5.1 --- Protocol 1- Dose effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.30 / Chapter 2.3.5.2 --- Protocol 2 - Time effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.30 / Chapter 2.3.5.3 --- Protocol 3 - Effect of co-incubation of LDL and copper(ll) sulphate on acetylcholine-induced vasorelaxation --- p.31 / Chapter 2.3.5.4 --- Protocol 4 - Effect of oxidized LDL on selected vasodilators --- p.32 / Chapter 2.3.5.5 --- Protocol 5 - Effect of pretreatment of L-arginine on oxidized LDL impaired -endothelium-induced relaxation --- p.32 / Chapter 2.3.5.6 --- Protocol 6 - Effect of a -tocopherol on oxidized LDL-damaged acetylcholine- induced vasorelaxation --- p.33 / Chapter 2.3.5.7 --- Protocol 7 - Effect of a -tocopherol on LDL and copper(ll) sulphate- induced endothelial dysfunction --- p.33 / Chapter 2.3.6 --- Western blot analysis of endothelial nitric oxide synthase (eNOS) protein --- p.34 / Chapter 2.3.7 --- Statistics --- p.35 / Chapter 2.4 --- Results --- p.36 / Chapter 2.4.1 --- Dose effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.36 / Chapter 2.4.2 --- Time effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.36 / Chapter 2.4.3 --- Effect of co-incubation of LDL and copper(II) sulphate on acetylcholine- induced vasorelaxation --- p.39 / Chapter 2.4.4 --- Effect of oxidized LDL on selected vasodilators --- p.41 / Chapter 2.4.5 --- Effect of pretreatment of L-arginine on oxidized LDL impaired- acetylcholine-induced relaxation --- p.41 / Chapter 2.4.6 --- Effect of a-tocopherol on oxidized LDL-damaged acetylcholine- induced vasorelaxation --- p.48 / Chapter 2.4.7 --- Effect of a-tocopherol on LDL and copper(II) sulphate-induced endothelial dysfunction --- p.50 / Chapter 2.4.8 --- eNOS Protein expression --- p.50 / Chapter 2.5 --- Discussion --- p.53 / Chapter CHAPTER 3 --- EFFECTS OF LDL INJECTION ON THE ENDOTHELIAL FUNCTION OF RATS / Chapter 3.1 --- Introduction --- p.58 / Chapter 3.2 --- Objective --- p.60 / Chapter 3.3 --- Methods and Materials --- p.61 / Chapter 3.3.1 --- Preparation of Drugs --- p.61 / Chapter 3.3.2 --- Preparation of LDL --- p.61 / Chapter 3.3.3 --- Animal Treatment --- p.61 / Chapter 3.3.4 --- Serum lipid and lipoprotein determinations --- p.62 / Chapter 3.3.5 --- Measurement of serum MDA level by TBARS assay --- p.62 / Chapter 3.3.6 --- Preparation of aorta --- p.62 / Chapter 3.3.7 --- Organ bath experiment --- p.63 / Chapter 3.3.8 --- Statistics --- p.64 / Chapter 3.4 --- Result --- p.65 / Chapter 3.4.1 --- Growth and food intake --- p.65 / Chapter 3.4.2 --- "Effect of LDL injection on serum TC, TG and HDL-C" --- p.65 / Chapter 3.4.3 --- Effect of LDL injection on non-HDL-C and ratio of non-HDL-C to HDL-C --- p.65 / Chapter 3.4.4 --- Serum MDA level --- p.68 / Chapter 3.4.5 --- Phenylephrine-induced contraction --- p.70 / Chapter 3.4.6 --- Endothelium-dependent and -independent relaxation --- p.75 / Chapter 3.5 --- Discussion --- p.79 / Chapter CHAPTER 4 --- EFFECTS OF INDIVIDUAL COMPONENT OF OXIDIZED LDL ON ENDOTHELIUM-DEPENDENT RELAXATION / Chapter 4.1 --- Introduction --- p.83 / Chapter 4.2 --- Objectives --- p.85 / Chapter 4.3 --- Materials and methods --- p.86 / Chapter 4.3.1 --- Preparation of drugs --- p.86 / Chapter 4.3.2 --- Preparation of human native LDL and oxidized LDL --- p.86 / Chapter 4.3.3 --- GC analysis of fatty acid composition in LDL --- p.86 / Chapter 4.3.4 --- TBARS assay analysis of MDA content in LDL --- p.87 / Chapter 4.3.5 --- GC analysis of cholesterol oxidation products in LDL --- p.89 / Chapter 4.3.6 --- Thin-layer chromatography analysis of LPC in LDL --- p.91 / Chapter 4.3.7 --- Preparation of aorta --- p.92 / Chapter 4.3.8 --- Measurement of Isometric Force in vitro --- p.92 / Chapter 4.3.8.1 --- Protocol 1- effect of LPC on acetylcholine-induced vasorelaxation --- p.92 / Chapter 4.3.8.2 --- Protocol 2- effect of cholesterol oxidation products on acetylcholine-induced vasorelaxation --- p.92 / Chapter 4.3.8.3 --- Protocol 3- effect of oxidized fatty acids on acetylcholine-induced vasorelaxation --- p.93 / Chapter 4.3.9 --- Statistics --- p.93 / Chapter 4.4 --- Results --- p.94 / Chapter 4.4.1 --- Compositional differences between native LDL and oxidized LDL.… --- p.94 / Chapter 4.4.2 --- Effect of LPC on endothelium-dependent relaxation --- p.98 / Chapter 4.4.3 --- Effect of COPs on endothelium-dependent relaxation --- p.98 / Chapter 4.4.4 --- Effect of oxidized fatty acids on endothelium-dependent relaxation --- p.101 / Chapter 4.5 --- Discussion --- p.103 / Chapter CHAPTER 5 --- EFFECTS OF DIETARY OXIDIZED CHOLESTEROL ON BLOOD CHOLESTEROL LEVEL IN HAMSTERS / Chapter 5.1 --- Introduction --- p.107 / Chapter 5.2 --- Objectives --- p.111 / Chapter 5.3 --- Materials and Methods --- p.112 / Chapter 5.3.1 --- Preparation of Oxidized Cholesterol --- p.112 / Chapter 5.3.2 --- Diet preparation --- p.112 / Chapter 5.3.3 --- Animals --- p.113 / Chapter 5.3.4 --- Serum lipid and lipoprotein determinations --- p.116 / Chapter 5.3.5 --- GC analysis of cholesterol and cholesterol oxidation products on organs --- p.116 / Chapter 5.3.6 --- Extraction of neutral and acidic sterols from fecal samples --- p.117 / Chapter 5.3.6.1 --- Determination of neutral sterols --- p.117 / Chapter 5.3.6.2 --- Determination of acidic sterols --- p.117 / Chapter 5.3.6.3 --- GLC analysis of neutral and acidic sterols --- p.118 / Chapter 5.3.7 --- Organ bath experiment --- p.121 / Chapter 5.3.7.1 --- Preparation of aorta --- p.121 / Chapter 5.3.7.2 --- Aortic relaxation --- p.121 / Chapter 5.3.8 --- Analysis of the total area of atherosclerotic plaque on aorta --- p.122 / Chapter 5.3.9 --- Statistics --- p.122 / Chapter 5.4 --- Results --- p.123 / Chapter 5.4.1 --- GC of oxidized cholesterol --- p.123 / Chapter 5.4.2 --- Growth and food intake --- p.123 / Chapter 5.4.3 --- "Effect of non-oxidized and oxidized cholesterol on serum TC, TG and HDL-C" --- p.123 / Chapter 5.4.4 --- Effect of non-oxidized and oxidized cholesterol on non-HDL-C and ratio of non-HDL-C to HDL-C --- p.124 / Chapter 5.4.5 --- Effect ofnon-oxidized and oxidized cholesterol on concentration of hepatic cholesterol --- p.128 / Chapter 5.4.6 --- Effect of non-oxidized and oxidized cholesterol on concentration of cholesterol oxidation products accumulated in liver --- p.128 / Chapter 5.4.7 --- Effect of non-oxidized and oxidized cholesterol on concentration of brain and aortic cholesterol --- p.128 / Chapter 5.4.8 --- Effect of non-oxidized and oxidized cholesterol on fecal neutral and acidic sterols --- p.129 / Chapter 5.4.9 --- Effect of non-oxidized and oxidized cholesterol on aortic relaxation --- p.135 / Chapter 5.4.10 --- Effect of non-oxidzied and oxidized cholesterol on area of atherosclerotic plaque --- p.137 / Chapter 5.5 --- Discussion --- p.139 / Chapter CHAPTER 6 --- CONCLUSION --- p.143 / REFERENCES --- p.146