| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2729200 | The Journal of Pain | 2008 | 8 Pages |
Visceral injury has been shown to alter somatic sensitivity, but little is known about the effect of somatic insult on the viscera. In the present study, we examined (1) the effect of colon inflammation on somatic sensitivity and (2) the affect of hind paw incision on colon sensitivity. After intracolonic administration of trinitrobenzene sulfonic acid (TNBS) or zymosan, visceromotor responses to colorectal distension were increased to post-treatment day 8. Mechanical withdrawal thresholds in the hind paw were decreased in TNBS- and in zymosan-treated rats until post–intracolonic treatment day 2. There was no change in hind paw heat withdrawal latency in either group. Plantar incision of the hind paw resulted in a decrease in both hind paw mechanical withdrawal threshold and heat withdrawal latency and significantly increased the visceromotor response to colorectal distension from postincision days 1 to 8. The colon hypersensitivity was of longer duration than hyperalgesia at the site of hind paw incision. These results support the hypothesis that somatic injury and visceral inflammation can alter central processing of visceral and somatic inputs, respectively.PerspectiveSurgical procedures are common and typically associated with hyperalgesia at and around the site of incision. This report establishes in a model of postsurgical pain and hyperalgesia that a long-lasting visceral hypersensitivity may also accompany postsurgical hyperalgesia.
