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Electronic Letters to:

Editorials:
J. P. Williams and D. G. Lambert
Editorial II: Opioids and the neuroimmune axis
Br. J. Anaesth. 2005; 94: 3-6 [Full text] [PDF]
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[Read E-letter] Opioids and the neuroimmune axis
Michal R. Pijak   (24 May 2005)

Opioids and the neuroimmune axis 24 May 2005
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Michal R. Pijak,
Consultant in Rheumatology and Clinical Immunology
University Hospital, 83101 Bratislava, Slovakia

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Re: Opioids and the neuroimmune axis

The editorial by Williams and Lambert (1) on opioids and the neuroimmune axis is of considerable interest to me because it substantiates the results of my experiments concerning sensory modulation of neurogenic inflammation (2, 3). In this contention I wish to point out at my unpublished study presented nearly 20 years ago at the 2nd World Conference on Inflammation in Monte-Carlo (4). To my knowledge this report, which abstract I am presenting below, was the first demonstrating enhanced inflammatory response after administration of opiate antagonist in humans.

“Inhibition of experimental inflammation by morphine is a well known fact an there is evidence that inflammatory response is enhanced during the withdrawal of opioid drugs. These observations may suggest that endogenous opioids are involved not only in pain control but also in involuntary reactions to injury. Naloxone, then, might facilitate responding by blocking this control. In six healthy volunteers intradermal injection injection of 0.01 ml of 1:1000 histamine base was made to the inner part of forearm and skin reaction was examined at 10 min intervals. One hour later the same procedure was performed on the other forearm but five minutes prior to histamin injection of Naloxone (4mg in 10 ml solution) was injected intravenously. Additional 12 persons (control group) were studied in an identical manner using saline solution instead of naloxone. The area of wheal but not flare after pretreatment with naloxone was larger and duration of reaction was longer then in control forearm in all subjects. No significant differences were observed in the control group. These results suggest that endogenous opioids are involved in the control of neurogenic component of inflammation. As long as this negative feed-back control is intact, the neurogenic inflammatory process is self-limiting. Vice-versa, when it breaks down, the process may remain self-perpetuated, e.g. because nociceptive neurons in dorsal root ganglion that manufacture substance P continue responding to irritation of peripheral terminals induced by chemical mediators released from mast cells which are further stimulated by substance P.”

References

1. Williams JP, Lambert DG. Opioids and the neuroimmune axis. Br J Anaesth 2005;94:3-6.

2. Pijak MR: Die Wirkung der Transcutanen Elektrostimulation (TES) auf die Histaminreaktion der Haut (HRH). Z Phys Med Baln Med Klin 1985;14(5):286-287.

3. Pijįk MR: Inhibition of immediate hypersensitivity skin reactions by non-painful transcutaneous electrical nerve stimulation (TENS). Scand J Immunol, 2001; 54(suppl 1):113.

4. Pijak MR: Naloxone enhances neurogenic inflammation. Abstract No. A154. 2nd World Conference on Inflammation.; 1986 March 19-22; Monte -Carlo, Monaco.

Conflict of Interest:

None declared