Modulation of peripheral endogenous opioid analgesia by central afferent blockade
Male; Analgesics; Animals; Rats; Injections; Immunohistochemistry; Spinal; Enkephalin; beta-Endorphin/metabolism; Wistar; Pain Threshold/drug effects; Neurons; Afferent/drug effects; Central Nervous System/drug effects; Endorphins/metabolism/physiology; Flow Cytometry; Foot/pathology; Inflammation/pathology; Methionine/metabolism; Morphine/administration & dosage/pharmacology; Opioid/administration & dosage/pharmacology; Peripheral Nerves/drug effects; Psychomotor Performance/drug effects
BACKGROUND: Peripheral tissue injury causes a migration of opioid peptide-containing immune cells to the inflamed site. The subsequent release and action of these peptides on opioid receptors localized on peripheral sensory nerve terminals causes endogenous analgesia. The spinal application of opioid drugs blocks the transmission of nociceptive information from peripheral injury. This study investigates the influence of exogenous spinal opioid analgesia on peripheral endogenous opioid analgesia. METHODS: Six and forty-eight hours after initiation of continuous intrathecal morphine infusion and administration of Freund's complete adjuvant into the hind paw of rats, antinociceptive and antiinflammatory effects were measured by paw pressure threshold, paw volume, and paw temperature, respectively. Inflammation and quantity of opioid-containing cells were evaluated by immunocytochemistry and flow cytometry. Cold water swim stress-induced endogenous analgesia was examined 24 h after discontinuation of intrathecal morphine administration. RESULTS: Intrathecal morphine (10 micro g/h) resulted in a significant and stable increase of paw pressure threshold ( P 0.05). At 48 but not at 6 h after Freund's complete adjuvant, the number of beta-endorphin-containing cells and cold water swim-induced antinociception were significantly reduced in intrathecal morphine-treated rats compared with those treated with intrathecal vehicle ( P< 0.05). CONCLUSIONS: These findings suggest an interplay of central and peripheral mechanisms of pain control. An effective central inhibition of pain apparently signals a reduced need for recruitment of opioid-containing immune cells to injured sites.
2003
Schmitt TK; Mousa SA; Brack A; Schmidt DK; Rittner HL; Welte M; Schafer M; Stein C
Anesthesiology
2003
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1097/00000542-200301000-00030" target="_blank" rel="noreferrer">10.1097/00000542-200301000-00030</a>
The control of pain in peripheral tissue by opioids
Humans; Animals; Biomarkers of Pain; Pain/drug therapy; Receptors; Opioid/drug effects; Narcotics/therapeutic use; Neurons; Afferent/drug effects; Peripheral Nervous System Diseases/drug therapy/physiopathology
1995
Stein C
The New England Journal Of Medicine
1995
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1056/nejm199506223322506" target="_blank" rel="noreferrer">10.1056/nejm199506223322506</a>