Surgical autonomic denervation results in altered colonic motility: an explanation for low anterior resection syndrome?

Published

Journal Article

BACKGROUND: We hypothesized that the bowel dysfunction known as low anterior resection syndrome is caused by denervation of the left colon. The purpose of this study is to determine how surgical denervation changes left colon motility and to identify the mechanism of this change. MATERIALS AND METHODS: Strain gauge transducers were implanted on the serosal surface of the descending colon of male SD rats (250-300 g). After a 2-h baseline recording, motility was recorded for another 2 h after either simple left colon manipulation (n = 6) or surgical left colon denervation (n = 6). Various pharmacologic agents were then administered before denervation to determine the mechanism by which denervation changed left colon motility. Changes in motility were calculated by determining a % motility index (MI) (%MI = MI posttreatment/MI baseline) with significance defined as P < .05. RESULT: Denervation resulted in an increased mean %MI (128.8 +/- 15.4) compared with simple manipulation of the bowel, which decreased mean %MI (87.9 +/- 25.3) (P < .05). In the second set of experiments, both guanethidine and phentolamine increased mean %MI after injection (P < .05), but no additional increase of %MI occurred after denervation (P < .05). However, propranolol produced no increase of motility after injection and it did not affect the increase in motility observed after denervation (P < .05). CONCLUSION: Surgical denervation of the left colon results in a significant increase in motility. Pharmacologically, this increase seems to be the result of destruction of an inhibitory alpha-sympathetic pathway. This increased motility may contribute to low anterior resection syndrome.

Full Text

Duke Authors

Cited Authors

  • Lee, WY; Takahashi, T; Pappas, T; Mantyh, CR; Ludwig, KA

Published Date

  • June 2008

Published In

Volume / Issue

  • 143 / 6

Start / End Page

  • 778 - 783

PubMed ID

  • 18549894

Pubmed Central ID

  • 18549894

Electronic International Standard Serial Number (EISSN)

  • 1532-7361

Digital Object Identifier (DOI)

  • 10.1016/j.surg.2008.03.014

Language

  • eng

Conference Location

  • United States