Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 1 July 2008
Vol. 1, Issue 26, p. ec236
[DOI: 10.1126/scisignal.126ec236]


Pharmacology Anesthesia Increases Postoperative Pain

Nancy R. Gough

Science Signaling, AAAS, Washington, DC 20005, USA

Patients often report a burning sensation when receiving intravenously delivered anesthetics, and respiratory irritation limits the dose of pungent inhalation anesthetics. Matta et al. show that the pungent volatile anesthetics isoflurane and desflurane, as well as the intravenous anesthetics propofol and etomidate (collectively referred to as the noxious general anesthetics), activated TRPA1 channels, which are members of the transient receptor potential family that are present on a large proportion of peripheral nociceptive sensory neurons. The nonpungent volatile anesthetics halothane and sevoflurane did not. Electrophysiology experiments revealed that the noxious general anesthetics activated TRPA1 channels, but not TRPV1 or TRPM8 channels, when the channels were heterologously expressed in cultured cells. Calcium imaging experiments on neurons cultured from dorsal root ganglia indicated that these noxious general anesthetics activated nociceptive neurons containing TRPA1. Cells isolated from TRPA1-null mice failed to respond to the noxious general anesthetics. The noxious general anesthetics activated the channels in cell-free patches, which suggests that these drugs may interact directly with the channel and do not require second messenger signaling for channel regulation. The pain response triggered by propofol administered to mice required TRPA1, and coadministration of a neurogenic irritant with isoflurane triggered more swelling than was observed with the irritant alone. Thus, although these central nervous system depressants are important for induction of surgical anesthesia, choosing a general anesthetic that does not activate TRPA1 may minimize postoperative pain and inflammation.

J. A. Matta, P. M. Cornett, R. L. Miyares, K. Abe, N. Sahibzada, G. P. Ahern, General anesthetics activate a nociceptive ion channel to enhance pain and inflammation. Proc. Natl. Acad. Sci. U.S.A. 105, 8784-8789 (2008). [Abstract] [Full Text]

Citation: N. R. Gough, Anesthesia Increases Postoperative Pain. Sci. Signal. 1, ec236 (2008).

Science Signaling Podcast: 05 August 2008.
N. R. Gough and A. M. VanHook (2008)
Science Signaling 1, pc7
   Abstract »    Full Text »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882