Rectal inhibition by inferior rectal nerve stimulation in dogs: recognition of a new reflex--the 'voluntary anorectal inhibition reflex'
- PMID: 11338072
- DOI: 10.1097/00042737-200104000-00019
Rectal inhibition by inferior rectal nerve stimulation in dogs: recognition of a new reflex--the 'voluntary anorectal inhibition reflex'
Abstract
Objective: The effect of inferior rectal nerve (IRN) stimulation on the rectum was studied, postulating that nerve stimulation might inhibit rectal contractility and could thus be used in the management of defecation disorders.
Method: The IRN was exposed through a para-anal incision in 12 dogs (18.2 +/- 3.3 SD kg, seven male, five female) and a cuff-type electrode was applied to the nerve. A balloon introduced into the rectum was filled with saline in increments of 5 ml. The rectal and rectal neck (anal canal) pressures, and the electromyographic (EMG) activity of the external anal sphincter (EAS) and Internal anal sphincter (IAS) were recorded until the balloon was expelled to the exterior. The test was repeated until the expulsion volume was reached, and the IRN was stimulated (pulse width 200 mu/s, charge density 2 to 6 microCi/cm2 per phase). The test was performed again following individual anaesthetization of the EAS and the IAS.
Results: At a mean rectal distending volume of 38.3 +/- 2.3 ml, the rectal pressure increased (P < 0.01), rectal neck pressure declined (P < 0.01), the EAS and IAS EMGs disappeared, and the balloon was expelled. IRN stimulation at a distending volume of 38.3 +/- 2.3 ml increased the EMG activity of the EAS, whereas the rectal pressure and IAS EMG did not change (P > 0.05) and the balloon was not expelled. With IRN stimulation at the distending volume of 38.3 +/- 2.3 ml while the EAS was anaesthetized, the rectal pressure increased (P < 0.01), rectal neck pressure diminished, IAS EMG activity disappeared, and the balloon was expelled. Upon repetition of IRN stimulation during anaesthetization of the IAS, the rectal pressure remained high and the balloon was not expelled.
Conclusion: It is suggested that the EAS produces continence by a twofold action. The EAS prevents IAS relaxation on rectal contraction, with a resulting rectal relaxation. A reflex relationship is postulated to exist between failure of the IAS to relax and rectal relaxation. We call this reflex relationship 'voluntary anorectal inhibition reflex'. Secondly, the EAS mechanically compresses the rectal neck. It seems that contraction of the EAS, which is a striated muscle, mechanically occludes the rectal neck for a few seconds--enough for the rectum to relax in a reflex manner as an effect of the voluntary anorectal inhibition reflex.
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