scholarly journals Persistent Catechol-O-methyltransferase–dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors

2016 ◽  
Vol 124 (5) ◽  
pp. 1122-1135 ◽  
Author(s):  
Brittney P. Ciszek ◽  
Sandra C. O’Buckley ◽  
Andrea G. Nackley
Keyword(s):  
Chronic Pain ◽  
Mechanical Stimuli ◽  
Chronic Pain Patients ◽  
Β Adrenergic Receptors ◽  
Pain Patients ◽  
Thermal Stimuli ◽  
Pump Implantation ◽  
Pharmacologic Inhibition ◽  
Adrenalectomized Rats ◽  
Intact Rats

Abstract Background Patients with chronic pain disorders exhibit increased levels of catecholamines alongside diminished activity of catechol-O-methyltransferase (COMT), an enzyme that metabolizes catecholamines. The authors found that acute pharmacologic inhibition of COMT in rodents produces hypersensitivity to mechanical and thermal stimuli via β-adrenergic receptor (βAR) activation. The contribution of distinct βAR populations to the development of persistent pain linked to abnormalities in catecholamine signaling requires further investigation. Methods Here, the authors sought to determine the contribution of peripheral, spinal, and supraspinal βARs to persistent COMT-dependent pain. They implanted osmotic pumps to deliver the COMT inhibitor OR486 (Tocris, USA) for 2 weeks. Behavioral responses to mechanical and thermal stimuli were evaluated before and every other day after pump implantation. The site of action was evaluated in adrenalectomized rats receiving sustained OR486 or in intact rats receiving sustained βAR antagonists peripherally, spinally, or supraspinally alongside OR486. Results The authors found that male (N = 6) and female (N = 6) rats receiving sustained OR486 exhibited decreased paw withdrawal thresholds (control 5.74 ± 0.24 vs. OR486 1.54 ± 0.08, mean ± SEM) and increased paw withdrawal frequency to mechanical stimuli (control 4.80 ± 0.22 vs. OR486 8.10 ± 0.13) and decreased paw withdrawal latency to thermal heat (control 9.69 ± 0.23 vs. OR486 5.91 ± 0.11). In contrast, adrenalectomized rats (N = 12) failed to develop OR486-induced hypersensitivity. Furthermore, peripheral (N = 9), but not spinal (N = 4) or supraspinal (N = 4), administration of the nonselective βAR antagonist propranolol, the β2AR antagonist ICI-118,511, or the β3AR antagonist SR59230A blocked the development of OR486-induced hypersensitivity. Conclusions Peripheral adrenergic input is necessary for the development of persistent COMT-dependent pain, and peripherally-acting βAR antagonists may benefit chronic pain patients.

The effect of experimentelly induced painful thermal stimuli on chronic pain patients

Pain ◽  
1987 ◽  
Vol 30 ◽  
pp. S312
Author(s):  
C. E. Elger ◽  
H. G. Berwald ◽  
M. Horstmann ◽  
A. C. Ludolph
Keyword(s):  
Chronic Pain ◽  
Chronic Pain Patients ◽  
Pain Patients ◽  
Thermal Stimuli

scholarly journals The Short-Term Kinetics of sICAM-1 after Induction of Acute Experimental Pain in Healthy Volunteers

2021 ◽  
Vol 10 (9) ◽  
pp. 2021
Author(s):  
Philipp Lüke ◽  
Eduard Kraft ◽  
Shahnaz Christina Azad
Keyword(s):  
Chronic Pain ◽  
Pain Intensity ◽  
Experimental Pain ◽  
Heat Pain ◽  
Short Term ◽  
Initial Values ◽  
Chronic Pain Patients ◽  
Pain Patients ◽  
Kinetics Of ◽  
Thermal Stimuli

Intercellular adhesion molecule-1 (ICAM-1) mediates extravasation of leukocytes, releasing proinflammatory cytokines or endogenous opioids in the inflamed tissue. Thus, ICAM-1 is a crucial component of peripheral antinociception. Previously, we demonstrated a significant correlation between the soluble form of ICAM (sICAM-1) in serum and pain intensity reported by chronic pain patients. The present study examines the role and kinetics of sICAM-1 in experimentally induced acute pain. Three groups of 10 subjects were exposed to 10 min of high (capsaicin-enhanced) or low-intensity heat pain or cold pain, respectively. Thermal stimuli were induced using a device for quantitative sensory testing. Topical capsaicin significantly increased heat pain intensity without the risk of thermal tissue damage. Pain intensity was recorded every minute during testing. sICAM-1 concentrations in serum were determined by ELISA before, immediately after, and 60 min after test termination. Among all experimental groups, sICAM-1 significantly decreased immediately after pain induction. After 60 min, sICAM-1 concentrations returned towards initial values. Interestingly, a linear correlation was found between the extent of sICAM-1 changes and the initial concentrations. Whereas high initial values led to a distinct decrease of sICAM-1, low concentrations tended to increase. There was no statistically significant correlation between levels or alterations of serum sICAM-1 and pain intensity reported by the test subjects. In contrast to our previous findings in chronic pain patients, the present results show that sICAM-1 values do not correlate with the intensity of acute experimental pain. However, we were able to detect short-term changes of sICAM-1 after induction of nociceptive thermal stimuli, suggesting that this marker is part of a demand-oriented homeostatically controlled system.

Pain Influences Several Levels of Attention

2005 ◽  
Vol 16 (4) ◽  
pp. 235-242 ◽  
Author(s):  
Astrid von Bueren Jarchow ◽  
Bogdan P. Radanov ◽  
Lutz Jäncke
Keyword(s):  
Chronic Pain ◽  
Divided Attention ◽  
Covert Attention ◽  
Attention Task ◽  
Attentional Deficits ◽  
Control Subjects ◽  
Chronic Pain Patients ◽  
Divided Attention Task ◽  
Pain Stimuli ◽  
Pain Patients

Abstract: The aim of the present study was to examine to what extent chronic pain has an impact on various attentional processes. To measure these attention processes a set of experimental standard tests of the “Testbatterie zur Aufmerksamkeitsprüfung” (TAP), a neuropsychological battery testing different levels of attention, were used: alertness, divided attention, covert attention, vigilance, visual search, and Go-NoGo tasks. 24 chronic outpatients and 24 well-matched healthy control subjects were tested. The control subjects were matched for age, gender, and education. The group of chronic pain patients exhibited marked deficiencies in all attentional functions except for the divided attention task. Thus, the data supports the notion that chronic pain negatively influences attention because pain patients` attention is strongly captivated by the internal pain stimuli. Only the more demanding divided attention task has the capability to distract the focus of attention to the pain stimuli. Therefore, the pain patients are capable of performing within normal limits. Based on these findings chronic pain patients' attentional deficits should be appropriately evaluated and considered for insurance and work related matters. The effect of a successful distraction away from the pain in the divided attention task can also open new therapeutic aspects.

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