Proefschrift--Groningen. / "Literature": p. 164-165.

Proefschrift--Groningen. / "Literature": p. 164-165.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Thesis (Ph.D.)--Boston University. / Rats were trained on three schedules of reinforcement, a sound aversive schedule, a light aversive schedule and a sound and light discrimination schedule. On the aversive schedules a press response terminated the aversive stimulus. On the discrimination schedule a response in the presence of either stimulus produced food. An auditory threshold was measured on this schedule. Following training the animals received electrolytic lesions in the ventral auditory system of the medulla. Following this they were tested on the behavioral schedules. The brain of each animal was then removed and impregnated with protargol for microscopic examination. Six rats received unilateral lesions, seven received bilateral lesions and six received sham operations. The results were as follows. Of the six animals who received unilateral lesions, one showed a substantial loss of the sound aversive behavior. Of the seven who received bilateral lesions five suffered a loss of the aversive behavior. Of these five, two had a substantial increase in the discriminative threshold. The behavior of the animals who received sham operations was essentially unaffected. There was a consistent relation between extensive damage to the large fiber pathway, the superior olivary pathway and the small fiber pathway and loss of the auditory aversive behavior. Destruction of the superior olivary pathway was not sufficient to produce a loss of the aversive behavior. The suggestion in the literature that the large fiber pathway is responsible for the maintenance of the aversive behavior was confirmed. Destruction of the superior olivary pathway either alone or in combination with destruction of the large fiber pathway did not materially change the auditory discriminative threshold. Destruction of all ventral acoustic pathways caused a loss of both aversive and discriminative auditory behaviors. Dorsal auditory pathways did not by themselves support either behavior. It has not been possible to determine if destruction of the small fiber pathway by itself can cause a loss of discriminative behavior. It was not possible to determine if return of the release response was due to the lesion or due to the loss of the press response.

No description available.

Orexin A and B, also known as hypocretin 1 and 2, are two recently isolated hypothalamic peptides. As orexin-containing neurons are strategically located in the lateral hypothalamus, which has long been suspected to play an important role in feeding behaviors, initial studies were focused on the involvement of orexins in positive food intake and energy metabolism. Recent studies implicate a more diverse biological role of orexins, which can be manifested at different level of the neuraxis. For example, canine narcolepsy, a disorder with close phenotypic similarity to human narcolepsy, is caused by a mutation of hypocretin receptor 2 gene. Results from our immunohistochemical and functional studies, which will be summarized here, suggest that the peptide acting on neurons in the rostral ventrolateral medulla augment sympathoexcitatory outflow to the spinal cord. This finding is discussed in the context of increased sympathetic activity frequently associated with obesity.

Acute kidney injury (AKI) is associated with renal medullary hypoxia. The medullary thick ascending limb (mTAL) in the renal outer medulla is most susceptible to hypoxic injury, due to marginal O2 supply and high O2 consumption. The objectives of this study were to document the earliest effect of hypoxia (8% O2 for 2.5 hrs) on the mTAL function, and to identify strategies to protect the mTAL from hypoxia. The earliest effect of hypoxia is large water diuresis, due to a fall in the medullary osmolality and increase in vasopressinase. Desmopressin acetate (dDAVP), a synthetic vasopressin analogue resistant to vasopressinase that may also increase O2 delivery, prevented water diuresis. A low dose (0.8mg/kg) of furosemide may significantly reduce the mTAL work without a large excretion of essential electrolytes. Large water diuresis may be diagnostically valuable in detecting renal tissue hypoxia, and dDAVP and furosemide may prevent AKI in the clinical setting.

Acute kidney injury (AKI) is associated with renal medullary hypoxia. The medullary thick ascending limb (mTAL) in the renal outer medulla is most susceptible to hypoxic injury, due to marginal O2 supply and high O2 consumption. The objectives of this study were to document the earliest effect of hypoxia (8% O2 for 2.5 hrs) on the mTAL function, and to identify strategies to protect the mTAL from hypoxia. The earliest effect of hypoxia is large water diuresis, due to a fall in the medullary osmolality and increase in vasopressinase. Desmopressin acetate (dDAVP), a synthetic vasopressin analogue resistant to vasopressinase that may also increase O2 delivery, prevented water diuresis. A low dose (0.8mg/kg) of furosemide may significantly reduce the mTAL work without a large excretion of essential electrolytes. Large water diuresis may be diagnostically valuable in detecting renal tissue hypoxia, and dDAVP and furosemide may prevent AKI in the clinical setting.

Wong Kwok Kui Wister. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 220-236). / ABSTRACT --- p.1 / OBJECTIVES FOR PROJECT --- p.4 / ABBREVIATIONS --- p.6 / Chapter CHAPTER 1 --- INTRODUCTORY LITERATURE REVIEWS / Chapter 1.1 --- Noradrenaline and adrenaline / Chapter 1.1.1 --- History --- p.8 / Chapter 1.2 --- The adrenal medulla / Chapter 1.2.1 --- The anatomy and microcirculation of the adrenal medulla --- p.10 / Chapter 1.2.2 --- Neuro-endocrine control of adrenal medullary secretion --- p.12 / Chapter 1.3 --- Dopamine / Chapter 1.3.1 --- Introduction --- p.14 / Chapter 1.3.2 --- Levels of DA in plasma and urine --- p.14 / Chapter 1.3.3 --- Origins of DA in the urine --- p.15 / Chapter 1.3.4 --- Control of renal DA production --- p.16 / Chapter 1.3.5 --- The actions of DA in the body --- p.17 / Chapter 1.3.6 --- The DA hypothesis --- p.17 / Chapter 1.3.7 --- Urinary NA and AD --- p.18 / Chapter 1.4 --- ACE inhibitors / Chapter 1.4.1 --- Brief review of the pharmacology of ACE inhibitors --- p.19 / Chapter 1.5 --- Catecholamine assays / Chapter 1.5.1 --- Introduction --- p.21 / Chapter 1.5.2 --- Chemistry --- p.22 / Chapter 1.5.3 --- Bioassay --- p.23 / Chapter 1.5.4 --- Colorimetry --- p.25 / Chapter 1.5.5 --- Fluorometry --- p.25 / Chapter 1.5.6 --- Radiochemical techniques --- p.27 / Chapter 1.5.7 --- Radioimmunoassay --- p.29 / Chapter 1.5.8 --- Chromatography --- p.30 / Chapter CHAPTER 2 --- METHODS - DEVELOPMENT OF A CATECHOLAMINE ASSAY & STABILITY STUDIES ON CATECHOLAMINES / Chapter 2.1 --- High performance liquid chromatography and electrochemical detection of catecholamines / Chapter 2.1.1 --- Introduction --- p.38 / Chapter 2.1.2 --- Basic equipment --- p.39 / Chapter 2.1.3 --- Stock aqueous CAT standards --- p.40 / Chapter 2.1.4 --- Mobile phase of HPLC-ECD --- p.40 / Chapter 2.1.5 --- Determination of mobile phase composition and flow rate --- p.41 / Chapter 2.1.6 --- Electrochemical detection --- p.43 / Chapter 2.1.7 --- Linearity and lowest detection limit of HPLC-ECD system --- p.49 / Chapter 2.1.8 --- Maintenance of HPLC-ECD system --- p.54 / Chapter 2.1.9 --- Discussion --- p.56 / Chapter 2.2 --- Sample pre-treatment & stability studies - Human urine / Chapter 2.2.1 --- Pre-treatment --- p.58 / Chapter 2.2.2 --- Analytical performance of the assay --- p.63 / Chapter 2.2.3 --- Stability studies --- p.85 / Chapter 2.2.4 --- Discussion --- p.101 / Chapter 2.2.5 --- Conclusions --- p.108 / Chapter 2.3 --- Sample pre-treatment & stability studies - Rat urine / Chapter 2.3.1 --- Pre-treatment --- p.111 / Chapter 2.3.2 --- Analytical performance of the assay --- p.111 / Chapter 2.3.3 --- Stability studies --- p.119 / Chapter 2.3.4 --- Discussion --- p.131 / Chapter 2.3.5 --- Conclusions --- p.133 / Chapter CHAPTER 3 --- "URINARY CREATININE, SODIUM AND POTASSIUM MEASUREMENTS" / Chapter 3.1 --- Introduction --- p.135 / Chapter 3.2 --- Method / Chapter 3.2.1 --- Urinary creatinine measurement --- p.135 / Chapter 3.2.2 --- Urinary sodium and potassium measurement --- p.136 / Chapter 3.3 --- Results / Chapter 3.3.1 --- Urinary creatinine measurement --- p.136 / Chapter 3.3.2 --- Urinary sodium and potassium measurement --- p.136 / Chapter 3.4 --- Discussion / Chapter 3.4.1 --- Urinary creatinine measurement --- p.136 / Chapter 3.4.2 --- Urinary sodium and potassium measurement --- p.137 / Chapter 3.5 --- Statistics --- p.138 / Chapter 3.6 --- Chemicals --- p.139 / Chapter CHAPTER 4 --- STUDIES ON URINARY EXCRETION OF CATECHOLAMINES IN MAN / Chapter 4.1 --- Population study on the relationships between dietary salt intake and urinary catecholamine output / Chapter 4.1.1 --- Introduction --- p.141 / Chapter 4.1.2 --- Method --- p.142 / Chapter 4.1.3 --- Results --- p.143 / Chapter 4.1.4 --- Discussion --- p.148 / Chapter 4.1.5 --- Conclusions --- p.149 / Chapter 4.2 --- The effect of oral salt loading on urinary catecholamine output / Chapter 4.2.1 --- Introduction --- p.149 / Chapter 4.2.2 --- Methods --- p.150 / Chapter 4.2.3 --- Results --- p.152 / Chapter 4.2.4 --- Discussion --- p.159 / Chapter 4.2.5 --- Conclusions --- p.161 / Chapter 4.3 --- The effects of perindopril on urinary catecholamine outputs / Chapter 4.3.1 --- Introduction --- p.162 / Chapter 4.3.2 --- Methods --- p.165 / Chapter 4.3.3 --- Results --- p.166 / Chapter 4.3.4 --- Discussion --- p.189 / Chapter 4.3.5 --- Conclusions --- p.190 / Chapter CHAPTER 5 --- STUDY ON URINARY EXCRETION OF CATECHOLAMINES AFTER ORAL ADMINISTRATION OF CAPTOPRIL TO RATS / Chapter 5.1 --- Introduction --- p.192 / Chapter 5.2 --- Methods --- p.192 / Chapter 5.3 --- Results --- p.193 / Chapter 5.4 --- Discussion --- p.210 / Chapter 5.5 --- Conclusions --- p.212 / Chapter CHAPTER 6 --- CONCLUSIONS --- p.214 / Chapter CHAPTER 7 --- FUTURE PROSPECTS --- p.216 / PUBLICATIONS TO DATE --- p.218 / ACKNOWLEDGEMENTS --- p.219 / REFERENCES --- p.220