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


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.


RESULTS
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).


CONCLUSIONS
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.
Lee
Woo Yong
WY
Department of Surgery, Sungkyunkwan University, Samsung Medical Center, Seoul, Korea.
Takahashi
Toku
T
Pappas
Theodore
T
Mantyh
Christopher R
CR
Ludwig
Kirk A
KA
D018663:Adrenergic Agents / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D017763:Autonomic Denervation / Q000009:adverse effects*; D001341:Autonomic Nervous System / Q000601:surgery*; D003106:Colon / Q000294:innervation* / Q000503:physiopathology*; D003109:Colonic Diseases, Functional / Q000209:etiology* / Q000503:physiopathology; D005769:Gastrointestinal Motility / Q000187:drug effects / Q000502:physiology*; D006145:Guanethidine / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D010528:Peristalsis / Q000187:drug effects / Q000502:physiology; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley
D018663:Adrenergic Agents; D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D011433:Propranolol; D010646:Phentolamine; D006145:Guanethidine