GUT HORMONE-RELEASE IN PATIENTS AFTER SPINAL-CORD INJURY

Gastrointestinal disorders including abdominal pain, abdominal distent ion, ileus, and constipation are common after spinal cord injury. In p hysiologic studies of patients with spinal cord injury, slow gastric e mptying, ileal dilation, and abnormal rectosigmoid motility have been found. However, it is not yet known whether abnormal gut hormone relea se is important in the development of these abnormalities. In healthy volunteers, there are postprandial increases in plasma peptide YY and motilin levels, which appear related to neural mechanisms. We hypothes ized that abdominal sympathetic pathways provide tonic inhibition of p eptide YY and motilin release and that postprandial increases in these gut hormones are mediated through spinal pathways. Fasting serum was obtained from normal volunteers, paraplegic patients, and tetraplegic patients. In studies in which patients were fed, serum was obtained fr om normal volunteers, paraplegic patients, and tetraplegic patients be fore and at 30-min intervals after a 280 kcal meal. Serum motilin and peptide YY levels were measured by radioimmunoassays. In fasting studi es, there was a trend (P = 0.23) toward increased fasting serum motili n in paraplegic patients, and this result did not support tonic inhibi tion of motilin release. Fasting peptide YY levels were not increased in spinal cord injury patients, which did not support tonic inhibition of peptide YY release. In fed studies, there were strong trends towar d postprandial increases in serum peptide YY in volunteers and paraple gic patients and a significant postprandial rise in serum peptide YY i n tetraplegic patients (P = 0.04). This was evidence against involveme nt of spinal pathways in postprandial release of peptide YY. There was a significant (P < 0.05) postprandial rise in serum motilin in volunt eers compared with spinal cord injury patients, consistent with previo us studies showing central nervous system control of motilin release. Abnormal small bowel and colonic motility in patients after spinal cor d injury could be related to decreased postprandial motilin release.