In the present study, long-term and short-term rat preparations were u
sed to develop a model for investigating external anal sphincter (EAS)
reflexes in intact and spinal cord-injured (SCI) rats, In this model,
EAS distension with an external probe elicits reflex contractions of
the EAS in intact, unanesthetized animals, At 2 h after spinal cord tr
ansection, none of the lesioned animals displayed EAS EMG activity, In
fact, once distended, the EAS was incapable of maintaining closure of
the anal orifice, Over a period of 4 days, spinalized animals develop
ed a hyperreflexia of the EAS response, By 48 h, the rectified, integr
ated EAS EMG was significantly elevated in comparison with nonlesioned
controls (EAS hyperreflexia), In addition, the duration of the EAS EM
G bursts in response to sphincter distension had significantly increas
ed, At 6 weeks after injury, the EAS was significantly hyperreflexic a
s measured by EMG burst duration and burst area, As with intact animal
s, posttransection EAS reflexes were highly anesthesia sensitive, Thes
e studies indicate that (1) brief distension of the anal orifice is su
fficient to evoke a physiologically relevant reflexive activation of t
he EAS in the rat, (2) the 2- to 24-h postinjury areflexia observed in
these experiments may be a suitable model for the study of spinal sho
ck, and (3) the observed EAS hyperreflexia after chronic SCI may repre
sent the permanent effects of removing descending inhibitory circuits
and segmental plasticity, making this reflex an appropriate measure of
defecatory dysfunction after spinal cord injury.