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This Article Full Text Full Text (PDF) All Versions of this Article: 554/1/227    most recent jphysiol.2003.056804v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Miao, F. J.-P. Articles by Levine, J. D. Search for Related Content PubMed PubMed Citation Articles by Miao, F. J.-P. Articles by Levine, J. D.

¹ NIH Pain Center ² Department of Oral and Maxillofacial Surgery ³ Department of Medicine ⁴ Department of Anatomy, University of California at San Francisco, San Francisco, CA 94143-0440, USA

Noxious stimuli inhibit inflammation by activating neuroendocrine stress axes, an effect that is potently attenuated by ongoing activity in subdiaphragmatic vagal afferents. Because this vagal afferent activity is carried in the coeliac and coeliac accessory branches of the subdiaphragmatic vagus, we tested the hypothesis that the activity arises from vagal afferents that innervate a proximal segment of the gastrointestinal tract. Surgical removal of the duodenum, but not the stomach, produces a marked (six orders of magnitude) leftward shift in the dose–response curve for intraplantar capsaicin-induced inhibition of synovial plasma extravasation induced by the potent inflammatory mediator bradykinin, in the knee joint; this is similar in magnitude to the inhibition produced by subdiaphragmatic or by coeliac plus coeliac accessory branch vagotomy. Fasting, to unload mechanically sensitive polymodal afferents in the proximal gastrointestinal tract, produces a similar leftward shift in the dose–response curve for the inhibitory effect of capsaicin, an effect that is reversed by balloon distension in the duodenum in fasted rats, while balloon distension postvagotomy had no effect. These results suggest that activation of mechanically sensitive vagal afferents in the duodenum contributes vagal afferent activity that modulates neuroendocrine control of the inflammatory response.

(Received 13 October 2003; accepted after revision 27 October 2003; first published online 31 October 2003)
Corresponding author J. D. Levine: NIH Pain Center UCSF, University of California at San Francisco, 521 Parnassus Avenue, C-522, Box 0440, San Francisco, CA 94134-0440, USA. Email: levine{at}itsa.ucsf.edu