beta-endorphin and Acute-Pain

Plasma levels of beta-endorphin (BE), an endogenous opioid analgesic, are often reported as they relate to acute and chronic pain outcomes. However, little is known about what resting plasma BE levels might reveal about functioning of the endogenous opioid antinociceptive system. This study directly examined associations between resting plasma BE and subsequent endogenous opioid analgesic responses to acute pain in 39 healthy controls and 37 individuals with chronic low back pain (LBP). Resting baseline levels of plasma BE were assessed. Next, participants received opioid blockade (8 mg naloxone i.v.) or placebo in a double-blind, randomized, crossover design. Participants then underwent two acute pain stimuli: finger pressure (FP) pain and ischaemic (ISC) forearm pain. Blockade effects (naloxone minus placebo pain ratings) were derived to index endogenous opioid analgesic function. In placebo condition analyses for both pain stimuli, higher resting BE levels were associated with subsequently greater reported pain intensity (p's < 0.05), with this effect occurring primarily in healthy controls (BE × Participant Type interactions, p's < 0.05). In blockade effect analyses across both pain tasks, higher resting plasma BE predicted less subsequent endogenous opioid analgesia (smaller blockade effects; p's < 0.05). For the ISC task, these links were significantly more prominent in LBP participants (BE × Participant Type Interactions, p's < 0.05). Results suggest that elevated resting plasma BE may be a potential biomarker for reduced endogenous opioid analgesic capacity, particularly among individuals with chronic pain. Potential clinical implications are discussed.

Topics: Acute Pain; Adult; Analgesia; beta-Endorphin; Chronic Pain; Cross-Over Studies; Double-Blind Method; Female; Humans; Low Back Pain; Male; Middle Aged; Naloxone; Narcotic Antagonists; Pain Measurement; Pain Threshold; Physical Stimulation

Acute pain and peripheral sensitization development after cautery disbudding was investigated in 33 calves administered preventive multimodal analgesia. The animals were assigned randomly to three groups: 1) Group SH (Control), undergoing sham disbudding at 1 and 4weeks of age; 2) Group ED (Early Disbudding), undergoing disbudding at 1week of age and sham disbudding at 4weeks of age; 3) Group LD (Late Disbudding), undergoing sham disbudding at 1week of age and disbudding at 4weeks of age. Physiological parameters (heart rate, respiratory rate, rectal temperature, invasive blood pressure, cortisol, β-endorphin, interleukin-1β, interleukin-6, tumor necrosis factor-α and haptoglobin plasmatic concentration), local variables (tactile sensitivity score, pressure pain thresholds and horn temperature), behavior and pain scores [multidimensional pain scale and visual analogue scale (VAS)] were assessed at baseline and at several pre-determined time points until 24h after disbudding. Tactile sensitivity score significantly and equally increased in both groups ED and LD and pressure pain thresholds significantly decreased in group LD until 24h after disbudding compared to group SH. Pain and VAS scores significantly and equally increased in both groups ED and LD until 24h after disbudding compared to group SH. No significant differences in physiological parameters, behavior and horn temperature were detected among groups. The present study suggests that acute pain and peripheral sensitization develop and do not differ in calves disbudded at 1week and 4weeks of age. Moreover, the use of physiological and behavioral parameters as sole indicators of acute pain might lead to improper conclusions and should be reassessed.

Topics: Acute Pain; Aging; Animals; beta-Endorphin; Blood Pressure; Body Temperature; Body Weight; Cattle; Cautery; Haptoglobins; Heart Rate; Horns; Hydrocortisone; Pain Measurement; Pain Threshold; Prospective Studies; Random Allocation; Respiration; Retrospective Studies; RNA, Messenger; Touch Perception; Tumor Necrosis Factor-alpha