Includes bibliographical references. / 3 v. : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / A selection of research papers, reviews, books and book chapters ... considered representative of the works by the author over the years 1958-1993. / Thesis (D.Sc.)--University of Adelaide, Dept. of Pathology, 1995

An experimental animal model was developed to study and define the relationship between the blood flow and the marrow cavity pressure of bone. The study was carried out in 24 rabbits and 32 dogs under nembutol anesthesia. A multichannel physiograph was used to record simultaneously the systemic blood pressure, bone blood flow, marrow cavity pressure of bone and time sequence. The systemic blood pressure was measured by cannulating a brachial or carotid artery. The bone blood flow was measured by cannulating the nutrient vein and/or the nutrient artery. The marrow cavity pressure was measured by inserting a steel cannula through a drill hole in the cortex into the marrow cavity. The bones studied were mainly the tibia and femur. During the normal control condition, the marrow cavity pressure was found to have a wide range from animal to animal. In the rabbits, the range was from 20 to 60 mm. Hg. (15 to 50 percent of the systemic blood pressure). In the dogs, it ranged from 40 to 120 mm. Hg. (20 to 90 percent of the systemic blood pressure). However, the systemic blood pressure, intramedullary pressure and nutrient venous outflow were remarkably constant in a control period, therefore, their changes under experimental conditions were readily recordable. Various factors affecting bone circulation were studied. If the femoral vein is occluded the marrow cavity pressure rises and the nutrient venous outflow increases indicating venous congestion of bone. Nutrient artery occlusion causes a sharp fall in marrow cavity pressure coupled with a marked decrease in the nutrient venous outflow. Adrenalin and noradrenalin intravenous infusions produce a fall in marrow cavity pressure coupled with a decreased bone blood flow, despite an elevation in the systemic blood pressure. Isoproterenol hydrochloride generally causes a fall in the systemic blood pressure, widening of the pulse pressure, a fall in the marrow cavity pressure and a decrease in the nutrient venous outflow. Electrical sympathetic stimulation produces a fall in the marrow cavity pressure and a decrease in bone blood flow. Lumbar sympathectomy causes a rise in the marrow cavity pressure and an increase in the bone blood flow. Skeletal muscle contraction produces bone venous congestion with elevation of the marrow cavity pressure and increased nutrient venous outflow. Muscular relaxation causes a momentary sharp fall in the marrow cavity pressure to sub control levels before returning to the normal pressure. It is concluded that the marrow cavity pressure is bone blood flow dependent and reflects well the changes in the hemodynamics of bone. The narrow pressure rises if the arterial blood supply to bone increases or the venous congestion occurs in bone. The marrow pressure falls if the arterial blood supply to bone decreases or the venous drainage of bone is facilitated. / Surgery, Department of / Medicine, Faculty of / Graduate

Due to the large volume and often conflicting results reported on postoperative endocrinological changes, the practicing surgeon has difficulty in finding applicable principles. A knowledge of these principles is however necessary for an understanding of the mechanisms responsible for survival of the organism after surgery. The results thus far thus far reported are based upon complicated methodology, and may appear to be more theoretical than of practical value. Studies based upon small laboratory animals are indeed statistically significant, but the interpretation of these results as applied to the patient is difficult. Controlled human studies have been few in number and only very small areas of the total picture have been studied. There are a few studies on surgical patients; however, the variable results make the conclusion questionable. Nevertheless, these studies have lent a realistic significance to the evaluation of the total postoperative state.

Thesis (M.Sc.)--Memorial University of Newfoundland, Faculty of Medicine, / Typescript. Bibliography: leaves 44-68.

Lin, Wenhua. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 162-190). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

by Ng Ka On. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 100-122). / Abstract --- p.i / Acknowledgement --- p.vi / Chapter 1. --- Introduction / Chapter 1.1 --- Testicular vasculature --- p.1 / Chapter 1.1.1 --- Structural organization --- p.1 / Chapter 1.1.2 --- Peculiar structural organization pertinent to the Consideration of function --- p.3 / Chapter 1.2 --- Importance of the blood flow to testicular function --- p.6 / Chapter 1.3 --- Measurement of testicular blood flow --- p.8 / Chapter 1.4 --- Control of testicular blood flow --- p.16 / Chapter 1.5 --- Adrenergic control in the testis --- p.18 / Chapter 1.5.1 --- Adrenergic innervation and source of catecholamines --- p.18 / Chapter 1.5.2 --- Regulation of testicular function --- p.20 / Chapter 1.5.3 --- Effect on testicular blood flow --- p.22 / Chapter 1.6 --- Serotonergic control in the testis --- p.23 / Chapter 1.6.1 --- Serotonergic innervation and source of serotonin --- p.23 / Chapter 1.6.2 --- Regulation of testicular function --- p.24 / Chapter 1.6.3 --- Effect on testicular blood flow --- p.25 / Chapter 1.7 --- Cholinergic control in the testis --- p.26 / Chapter 1.7.1 --- Cholinergic innervation and source of acetylcholine --- p.26 / Chapter 1.7.2 --- Regulation of testicular function --- p.28 / Chapter 1.7.3 --- Effect on testicular blood flow --- p.29 / Chapter 1.8 --- Aims of the study --- p.30 / Chapter 2. --- Materials and methods / Chapter 2.1 --- Animals --- p.31 / Chapter 2.2 --- Drugs and chemicals --- p.32 / Chapter 2.3 --- In vivo videomicroscopy method --- p.33 / Chapter 2.4 --- Hydrogen gas clearance method --- p.37 / Chapter 2.5 --- Data and statistical analyses --- p.45 / Chapter 3. --- Results / Chapter 3.1 --- Adrenergic control --- p.46 / Chapter 3.1.1 --- Response of the testicular subcapsular artery to adrenergic agonists and antagonists --- p.46 / Chapter 3.1.2 --- Effect of adrenergic agonists on testicular capillary blood flow --- p.57 / Chapter 3.2 --- Serotonergic control --- p.60 / Chapter 3.2.1 --- Response of the testicular subcapsular artery to serotonergic agonists and antagonists --- p.60 / Chapter 3.2.2 --- Effect of serotonergic agonists on testicular capillary blood flow --- p.69 / Chapter 3.3 --- Cholinergic control --- p.76 / Chapter 3.3.1 --- Response of the testicular subcapsular artery to serotonergic agonists and antagonists --- p.76 / Chapter 3.3.2 --- Effect of serotonergic agonists on testicular capillary blood flow --- p.79 / Chapter 4. --- Discussion / Chapter 4.1 --- Adrenergic control --- p.86 / Chapter 4.2 --- Serotonergic control --- p.90 / Chapter 4.3 --- Cholinergic control --- p.96 / Chapter 4.4 --- General discussion --- p.98 / Chapter 5. --- References --- p.100

Thesis (B.S.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 1980. / MICROFICHE COPY AVAILABLE IN ARCHIVES AND ENGINEERING. / Includes bibliographical references. / by Martin Raymond Prince. / B.S.

Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 1982. / MICROFICHE COPY AVAILABLE IN ARCHIVES AND ENGINEERING. / Includes bibliographical references. / by Martin Raymond Prince. / M.S.

Wan Din. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 155-175). / ABSTRACT --- p.1 / ACKNOWLEDGMENTS --- p.3 / LIST OF TABLES --- p.5 / LIST OF FIGURES --- p.7 / LIST OF ABBREVIATIONS --- p.8 / Chapter I. --- INTRODUCTION --- p.9 / Chapter I.A. --- Menopause --- p.9 / Chapter I.A.1. --- Definition of the Menopause --- p.9 / Chapter I.A.2. --- Pathophysiology of Ovarian Failure --- p.10 / Chapter I.B. --- Effects of the Menopause --- p.13 / Chapter I B.1. --- Acute Effects --- p.13 / Chapter I.B.2. --- Medium Term Effects --- p.14 / Chapter I.B.3. --- Chronic Effects --- p.15 / Chapter I.B.3.a. --- Osteoporosis --- p.15 / Chapter I.B.3.b. --- Coronary Artery Disease (CAD) --- p.17 / Chapter I.C. --- Management of the Menopause --- p.19 / Chapter I.C.1. --- Hormone Replacement Therapy --- p.21 / Chapter I.C.2. --- Oestrogens --- p.22 / Chapter I.C.2.a. --- Oral Oestrogens --- p.22 / Chapter I.C.3. --- Progestogens --- p.24 / Chapter I.C.3.a. --- Combined Oestrogen and Progestogen Therapy --- p.24 / Chapter I.C.4. --- Complications and Contraindications to Hormone Replacement Therapy --- p.26 / Chapter II. --- LITERATURE REVIEW --- p.34 / Chapter II.A. --- Atherosclerosis --- p.35 / Chapter II.B. --- Risk Factors for Coronary Artery Disease --- p.37 / Chapter II.B.1. --- Age and Sex --- p.38 / Chapter II.B.2. --- Age at Menopause --- p.38 / Chapter II.B.3. --- Family History --- p.38 / Chapter II.B.4. --- Serum Lipids --- p.39 / Chapter II.B.5. --- Blood Pressure --- p.39 / Chapter II.B.6. --- Smoking --- p.40 / Chapter II.B.7. --- Diabetes Mellitus --- p.40 / Chapter II.C. --- The Effect of the Menopause on Risk Factors for Coronary Heart Disease --- p.41 / Chapter II.C.1. --- The Effect of the Menopause on Lipids and Lipoproteins --- p.41 / Chapter II.C.2. --- The Effect of the Menopause on Glucose and Insulin Metabolism --- p.43 / Chapter II.C.3. --- The Effect of the Menopause on Coagulation --- p.44 / Chapter II.C.4. --- The Effect of the Menopause on the Arterial Wall --- p.45 / Chapter II.D. --- The Risk of Coronary Artery Disease After the Menopause --- p.46 / Chapter II.D.1. --- The Effect of the Menopause on Peripheral Vascular Disease (PVD) --- p.47 / Chapter II.E. --- The Effect of the Hormone Replacement Therapy on Coronary Artery Disease Risk --- p.49 / Chapter II.F. --- The Mechanism of Cardioprotection of Oestrogen --- p.63 / Chapter II.F.1. --- The Indirect Effect of the Hormone Replacement Therapy on the Cardiovascular System --- p.64 / Chapter II.F.1.a. --- The Effect on Lipids and Lipoproteins --- p.64 / Chapter II.F.1.b. --- The Effect on Coagulation and Fibrinolysis --- p.66 / Chapter II.F.1.c. --- The Effect on Insulin and Glucose Metabolism --- p.67 / Chapter II.F.2. --- The Direct Effects of the Hormone Replacement Therapy on the Cardiovascular System --- p.67 / Chapter II.F.2.a. --- The Effect of Oestrogen on Vascular Contractility --- p.68 / Chapter II.F.2.b. --- The Effect of Oestrogen on Endothelial Dysfunction --- p.69 / Chapter II.F.2.C. --- Other Possible Direct Actions of Oestrogen --- p.72 / Chapter II.G. --- The Effects of Oestrogen on Blood Flow --- p.73 / Chapter III. --- RESEARCH PLAN --- p.78 / Chapter III.A. --- Formation of Research Hypothesis --- p.78 / Chapter III B. --- Research Hypothesis --- p.80 / Chapter III.C. --- Plan of Studies --- p.81 / Chapter III.C.1. --- Pilot Study --- p.81 / Chapter III.C.2. --- Randomized Controlled Study --- p.81 / Chapter IV. --- METHODOLOGY --- p.84 / Chapter IV.A. --- Pilot Study --- p.84 / Chapter IV.B. --- Study Population --- p.87 / Chapter IV.B.1. --- Recruitment of Cases --- p.88 / Chapter IV.B.1.a. --- Patients' Consent --- p.88 / Chapter IV.B.1.b. --- Method of Recruitment --- p.88 / Chapter IV.B.1.e. --- Research Methodology --- p.89 / Chapter IV.C. --- Ethical Considerations --- p.90 / Chapter IV.D. --- Samples Size Calculation --- p.92 / Chapter IV.E. --- Statistical Analysis --- p.93 / Chapter IV.F. --- Physical Principles of the Measurement of Peripheral Resistance --- p.94 / Chapter IV.F.1. --- The Arterial Analogue Waveform --- p.97 / Chapter IV.F.2. --- Peak Systolic Velocity --- p.98 / Chapter IV.G. --- Measurement of Pulsatility Index --- p.100 / Chapter IV.G.1. --- Establishment of Methodologies Used to Measure Peripheral Blood Flow --- p.105 / Chapter IV.G.2. --- Training of the Investigator --- p.107 / Chapter IV.H. --- Assay for Serum Oestradiol --- p.108 / Chapter IV.H.1. --- Principles --- p.108 / Chapter IV.H.2. --- Reagents --- p.109 / Chapter IV.H.3. --- Sample Dilution --- p.111 / Chapter IV.H.4. --- Calibration --- p.112 / Chapter IV.H.5. --- Quality Control --- p.112 / Chapter IV.H.6. --- Assay Validation --- p.113 / Chapter V. --- RESULTS --- p.115 / Chapter V.A. --- Pilot Study --- p.115 / Chapter V.B. --- Study Population --- p.118 / Chapter V.B.1. --- Characteristics of the Patients at Recruitment --- p.120 / Chapter V.B.2. --- Doppler Measurements --- p.123 / Chapter V.B.3. --- Pulsatility Index and Serum Oestradiol --- p.135 / Chapter VI. --- DISCUSSION --- p.137 / Chapter VI.A. --- Overview --- p.132 / Chapter VI.A.1. --- The Pilot Study --- p.133 / Chapter VI.B. --- Study Population --- p.136 / Chapter VI.C. --- Doppler Ultrasound as a Measurement of Vascular Resistance and Blood Flow --- p.142 / Chapter VI.C.1. --- Reliability of Doppler Study --- p.143 / Chapter VI.D. --- Pulsatility Index and Hormone Replacement Therapy --- p.146 / Chapter VI.E. --- Effects of Oestrogen on Pulsatility Index --- p.150 / Chapter VI.F. --- Conclusions --- p.152 / Chapter VI.G. --- Future Directions --- p.153 / REFERENCES --- p.155 / APPENDIX1 --- p.176

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniv. / Bilagan utgöres av sammanfattnig på svenska med titeln: Fysiologiskt svar på arbete hos varmblodiga travhästar i relation till total blodvolym. Härtill 5 uppsatser.