Pain is a phenomenon of seminal interest to nursing; providing pain relief and easing suffering have been central activities within the domain of nursing practice since the profession's inception. Nurses understand that unrelieved pain brings with it a range of detrimental health effects, yet still to be explored is how pain, as an adrenergic and nociceptive stressor, might impact on inflammatory processes via its direct and indirect effects on cellular adhesion molecule (CAM) levels. Known responses of both the sympathetic nervous system to stress and the sensory nervous system to nociceptive stimuli suggest that pain could be an especially potent inducer of CAM expression. The proposed and revised application represents an expansion of the principal investigator's expertise in pain physiology to include the effects of pain on immune and inflammatory parameters via multidisciplinary collaboration with nationally-recognized immunologists, and completion of a pilot study exploring the effects of experimental pain on CAM levels in healthy controls. The roles of affective stress, epinephrine, norepinephrine, and interleukin-6 in pain-induced CAM expression will be described in a small sample using an experimental design with repeated measures and randomly ordered experimental (low-stress pain, high-stress pain) and control (no pain) conditions. Conceptualizing pain as a potent and unique stressor, its effects on concomitant inflammatory processes is clearly an area worthy of nursing investigation, with important health implications for many patients, particularly those suffering from chronic inflammatory diseases such as atherosclerosis, inflammatory bowel disease, and rheumatoid arthritis.
| Griffis, Charles A; Crabb Breen, Elizabeth; Compton, Peggy et al. (2013) Acute painful stress and inflammatory mediator production. Neuroimmunomodulation 20:127-33 |
