Gastric opioid peptides were characterized on the basis of their biochemical forms, sites of action, mode of release and effects on endocrine secretions of the stomach. Partial purification of opioid-like material from extracts of the corpus/antrum region of the rat stomach was carried out by Sephadex G-50 gel filtration chromatography followed by adsorption onto Amberlite XAD-2 resin. A single peak of opioid activity was determined by both radioreceptor assay (RRA) and bioassay. By high performance liquid chromatography (HPLC) this peak was resolved into several distinct components identified by their retention times and measurement by RRA and/or radioimmunoassay (RIA) as corresponding to methionine-enkephalin (met-enk), leucine-enkephalin (leu-enk), met-enk-arg-gly-leu, met-enk-arg-phe, as well as dynorphins 1-13, 1-17, and 1-8. Trypsin digestion of partially purified extracts resulted in an overall increase in opioid activity, suggesting the presence of larger, inactive forms which may function as precursors. The sites of opioid peptide action were inferred from autoradiographic demonstrations of the distribution of tritium-labelled opioid ligand binding. In the fundic region of the rat stomach mu- and delta-type opioid receptors were localized in the circular muscle, muscularis mucosae, suggesting that here the opioid peptides may be involved in the regulation of motor activity. In the corpus and antrum, these two opioid receptor types were found to be associated with the deepmuscular plexus in some areas, but predominantly in the submucosal plexus and mucosa where the opioid peptides may act to directly affect gastric endocrine and exocrine secretions. Mu-type ligands also bound to the circular muscle and myenteric plexus. Intestinal tissue demonstrated mu- and delta-opioid binding sites throughout the mucosa, extending to the tips of the villi, implicating their involvement in the regulation of intestinal fluid and electrolyte absorption. Using the isolated, perfused rat stomach preparation, endogenous leu-enk was found to be released into the gastric vasculature in response to potassium depolarization and to the nicotinic cholinergic agonist dimethyl-phenyl-piperazinium (DMPP). The muscarinic cholinergic agonist, methacholine, had no effect. Exogenously infused met-enk caused a prompt dose-dependent, naloxone sensitive inhibition of gastric inhibitory polypeptide (GlP)-stimulated somatostatin (SLI) secretion. A similar, but reduced effect was observed with dynorphin 1-13. Neither atropine nor hexamethonium affected the met-enk inhibition of GIP-stimulated SLI; therefore, it was proposed that met-enk was acting directly on the D-cells to inhibit somatostatin secretion, possibly by interacting with mucosal opioid receptors demonstrated by autoradiography. These results, demonstrating the presence of endogenous gastric opioid peptides of both the enkephalin and dynorphin families and the widespread distribution of opioid receptors in the gastrointestinal tract, coupled with the observed release of endogenous gastric leu-enk, and potent effects of opioid peptides on SLI secretion from the stomach, indicate that theopioid peptides are important physiological regulators of gastric and intestinal functions. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

by Yoswa Mbulalina Dambisya. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 204-248). / TITLE PAGE --- p.i / ABSTRACT --- p.ii / DEDICATION --- p.iv / ACKNOWLEDGEMENTS --- p.v / DECLARATION --- p.vi / LIST OF PUBLICATIONS --- p.vii / Chapter SECTION 1 --- GENERAL INTRODUCTION --- p.1 / Chapter Chapter 1. --- Factors in the aetiology of drug abuse --- p.3 / Chapter Chapter 2. --- An overview of the drug abuse situation in Hong Kong and Uganda --- p.16 / Chapter Chapter 3. --- Some aspects of opioid pharmacology --- p.29 / Chapter Chapter 4. --- Basic principles of pharmacokinetics --- p.65 / Chapter Chapter 5. --- The present investigation --- p.72 / Chapter SECTION 2 --- PHARMACODYNAMIC INTERACTIONS --- p.76 / Chapter Chapter 6. --- Effects of ephedrine and phenylpropanolamine on the antinociceptive effects of morphine and codeine --- p.77 / Chapter Chapter 7. --- Effects of ephedrine and phenylpropanolamine on opioid tolerance and dependence --- p.95 / Chapter Chapter 8. --- The role of adrenoceptors in the potentiation of opioid antinociception by ephedrine and phenylpropanolamine --- p.119 / Chapter Chapter 9. --- Effects of ephedrine and phenylpropanolamine on acute lethal toxicity of morphine and codeine --- p.131 / Chapter SECTION 3 --- PHARMACOKINETIC INTERACTIONS / Chapter Chapter 10. --- Effects of ephedrine and phenylpropanolamine on the plasma and brain disposition of morphine and codeine --- p.138 / Chapter Chapter 11. --- "Effects of ephedrine and phenylpropanolamine on the 24 h urinary excretion of codeine, morphine and their metabolites; and the disposition of codeine and morphine at steady state" --- p.162 / Chapter Chapter 12. --- "Summary of conclusion, and prospects for further studies" --- p.201 / REFERENCES --- p.204 / APPENDICES --- p.249

Thesis (Ph. D.)--University of Hong Kong, 1988.

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

by Chung-wing Chau. / Bibliography: leaves 170-183 / Thesis (M.Phil.) -- Chinese University of Hong Kong, 1983

by Kwok Kar Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1981. / Bibliography: leaves 140-154.

No description available.

Nursing activities directed at maintaining patient comfort incorporates time and energy. Nurses and researchers continue to search for adequate methods and information to quantify pain. The common mode of therapy is the administration of narcotics, which do not consistently relieve the pain described by traumatically injured patients. Discovery of endogenous opiates, such as β-endorphins, provided the potential for acquiring additional physiologic information regarding neuro-endocrine activities associated with pain. Consistent findings of concentrated β-endorphins in areas of the central nervous system previously identified as pain pathways prompted clinical researchers to determine β-endorphin levels in patients experiencing pain. The purposes of this investigation were to study β-endorphin levels in burn injured patients by describing: (1) the pattern of β-endorphin levels in burn injured patients during the first two weeks following injury, (2) the relationship between β-endorphin levels and the severity of the burn injury, (3) the relationship between analgesia taken by patients and the severity of the burn, and (4) the relationship between β-endorphin levels and the amount of analgesia given to the burn patient. Plasma samples for β-endorphin levels were obtained from 28 burned patients over a two-week interval. New England Nuclear ¹²⁵I β-Endorphin Kits were used to assay the plasma samples. In addition, information was tabulated from the patient's chart to complete the Burn Severity Index. Narcotic analgesia taken 24 hours before obtaining the blood sample were summarized and categorized according to the Equianalgesia Table. Descriptive and correlational statistics showed no significant relationships between β-endorphins over time, β-endorphins with burn severity, β-endorphins with the analgesia equivalency score, or burn severity with the analgesia equivalency scores. β-endorphin levels were elevated above normal in all 28 patients. Five patients displayed the anticipated declining pattern over the two-week interval post burn. Many erratic peaks and troughs in β-endorphin levels were observed with some peaks associated with clinical events. The findings of elevated β-endorphin levels have implications for nursing practice and provide stimulus for continued nursing research.

Thesis (M.A.)--York University, 1998. Graduate Programme in Kinesiology and Health Science. / Typescript. Includes bibliographical references (leaves 69-85). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pMQ39203.

Thesis--M. Phil., University of Hong Kong, 1984.