Ahmed Shafik1, Ali A Shafik, Ismail Ahmed. 1. Department of Surgery and Experimental Research, Faculty of Medicine, Cairo University, Cairo, Egypt. ashafik@ahmedshafik.org
Abstract
BACKGROUND/ OBJECTIVE: The present study investigated the hypothesis that rectal contraction is maintained by positive anorectal feedback elicited by continuous passage of stools through the rectal neck (anal canal), and that cessation of stool passage aborts rectal contraction. METHODS: Anal and rectal pressures were measured in 18 healthy volunteers (mean age = 38.6 years; 10 men, 8 women) during evacuation of saline infused into the rectum. Residual fluid volume was calculated. The test was repeated after separate application of lidocaine or bland gel to the rectal neck. RESULTS: On evacuation, fluid emanated from the rectal neck in continuous flow with no, or mild, straining. No residual saline was collected from 16 of 18 participants. After anal anesthetization, evacuation occurred in gushes induced with excessive straining; residual fluid was huge. Repetition of the test 2 hours after anesthetization produced the same results as before anesthetization. Bland gel applied to the rectal neck yielded results similar to those before gel application. CONCLUSION: Rectal contraction at defecation is suggested to be maintained by positive anorectal feedback evoked by continuous passage of stool through the rectal neck. This feedback appears to be affected through an anorectal excitatory reflex (ARR), which produces rectal contraction upon stimulation of anal stretch receptors. Abortion of this reflex by anal anesthetization seems to result in failure of the rectum to contract and in excessive straining to achieve rectal evacuation. ARR thus is suggested to be a second defecation reflex necessary to continue defecation, whereas the rectoanal inhibitory reflex is the primary reflex. The role of the ARR in pathogenesis of constipation and its utility in spinal cord injury need to be investigated.
BACKGROUND/ OBJECTIVE: The present study investigated the hypothesis that rectal contraction is maintained by positive anorectal feedback elicited by continuous passage of stools through the rectal neck (anal canal), and that cessation of stool passage aborts rectal contraction. METHODS: Anal and rectal pressures were measured in 18 healthy volunteers (mean age = 38.6 years; 10 men, 8 women) during evacuation of saline infused into the rectum. Residual fluid volume was calculated. The test was repeated after separate application of lidocaine or bland gel to the rectal neck. RESULTS: On evacuation, fluid emanated from the rectal neck in continuous flow with no, or mild, straining. No residual saline was collected from 16 of 18 participants. After anal anesthetization, evacuation occurred in gushes induced with excessive straining; residual fluid was huge. Repetition of the test 2 hours after anesthetization produced the same results as before anesthetization. Bland gel applied to the rectal neck yielded results similar to those before gel application. CONCLUSION: Rectal contraction at defecation is suggested to be maintained by positive anorectal feedback evoked by continuous passage of stool through the rectal neck. This feedback appears to be affected through an anorectal excitatory reflex (ARR), which produces rectal contraction upon stimulation of anal stretch receptors. Abortion of this reflex by anal anesthetization seems to result in failure of the rectum to contract and in excessive straining to achieve rectal evacuation. ARR thus is suggested to be a second defecation reflex necessary to continue defecation, whereas the rectoanal inhibitory reflex is the primary reflex. The role of the ARR in pathogenesis of constipation and its utility in spinal cord injury need to be investigated.