Lic-avh. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 3 uppsatser.

Graduation date: 1998

Graduation date: 1995

The purpose of this study was to elucidate relationships among habitual physical activity level, endogenous opioid level, postoperative opioid analgesic, and experiences of acute pain in response to the noxious stimulation of a subsequent orthopedic surgical procedure. Specifically, the study examined (1) the relationship between habitual activity and preoperative level of endogenous opioids in peripheral blood, and (2) whether habitual activity predicts perception of pain intensity or distress in response to a subsequent noxious stimulus. The study utilized a descriptive correlational design with causal modeling methodology to assess a five-stage theory. The convenience sample was comprised of 36 English-speaking adult subjects hospitalized for orthopedic surgeries. The theoretical concepts, acute pain intensity and distress, were indexed three times for each subject by visual analogue scales. Reliability and validity of the scales were assessed by correlation with concurrent pain measurements using randomized verbal descriptor lists. Multiple regression statistical techniques were used to estimate the theory; violations of causal modeling and statistical assumptions were assessed by residual analysis. For this sample, the strongest predictors of postoperative pain were the immediately preceding comparable indices of pain intensity or pain distress. Approximately 31% of the variance on postoperative analgesic was predicted by the combined effects of immediate postoperative pain and habitual activity. Although activity was not significantly related to endogenous opioid level in peripheral plasma, activity directly and positively influenced immediate postoperative pain intensity (Beta = .37), 24-hour pain distress (B = .27), and total opioid analgesic received in the initial 24 postoperative hours (Intensity B = .40; Distress B = .50). Endogenous opioid was significantly related only to immediate postoperative pain distress (B = -.26). More physically active patients reported greater immediate postoperative pain intensity and greater 24-hour pain distress; they received more postoperative exogenous analgesic. Incorporation of information about activity as a potential determinant of operative pain experiences would increase validity of nursing assessments on which pain interventions are based. Patients in acute pain would benefit from this improved scientific basis for pain assessment.

The endogenous opioid system may be involved in the pathogenesis of arrhythmias and produce deleterious haemodynamic effects in patients with myocardial ischaemia and/or cardiac failure. Plasma concentrations of β-endorphin, a potent opioid peptide, were elevated in 31/42 patients with acute myocardial infarction, 3/18 with unstable angina, 3/34 with chronic heart failure, 8/28 with acute heart failure and 10/14 with cardiogenic shock. (Met)enkephalin levels were generally normal. There was no independent statistical relationship between β-endorphin concentrations after myocardial infarction and the incidence of cardiac arrhythmias. In isolated myocardium, the opioid antagonists naloxone and nalmafene, and morphine, an agonist, all produced Class III antiarrhythmic effects. Naloxone enhanced the reduction in maximum upstroke velocity produced by hyperkalaemia and post-repolarization refractoriness developed. During myocardial ischaemia the Class III effects of naloxone were gradually lost but both racemic naloxone (active at opioid receptors) and d-naloxone (inactive) reduced the rate of rise of extracellular potassium concentration and preserved resting membrane potential. The fall in maximum upstroke velocity during ischaemia was enhanced by both compounds suggesting an additional Class I effect. In human studies, despite employing high doses of naloxone, it was only possible to show a minor prolongation of repolarization. In patients with coronary heart disease, naloxone administered by both intracoronary and intravenous routes had no effect on coronary blood flow. In patients with heart failure naloxone had no significant effects on a range of haemodynamic parameters, exercise performance or levels of dyspnoea and fatigue.

No description available.

Thesis (Ph.D)--Tufts University, 2000. / Adviser: Robin B. Kanarek. Submitted to the Dept. of Psychology. Includes bibliographical references (leaves 109-134). Access restricted to members of the Tufts University community. Also available via the World Wide Web;

Graduation date: 1996

No description available.

Thesis (Ph.D.)--Murdoch University, 2004. / Thesis submitted to the Division of Health Sciences. Bibliography: leaves 351-376.