Small bowel transplantation: Effects on function of nonadrenergic, noncholinergic nerves |
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Authors: | Michel M. Murr M.D. Michael G. Sarr M.D. |
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Affiliation: | (1) Department of Surgery, Mayo Clinic and Mayo Foundation, 200 First St. SW, 55905 Rochester, MN;(2) Gastroenterology Research Unit, Mayo Clinic and Mayo Foundation, 200 First St. SW, 55905 Rochester, MN |
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Abstract: | Previous work from our laboratory showed that spontaneous contractile activity of jejunal smooth muscle increases after small bowel transplantation. Our aim was to determine whether small bowel transplantation alters the function of nonadrenergic, noncholinergic (NANC) nerves. Seven groups of rats, (n ≥7 in each group) were studied as follows: 1 week after sham celiotomy and 1 week and 8 weeks after 45 minutes of ischemia/ reperfusion (IR1 and IR8), jejunal and ileal transection and reanastomosis (TR1 and TR8), or orthotopic small bowel transplantation (TX1 and TX8). Contractility of jejunal circular muscle strips was studied in vitro. Spontaneous contractile activity increased in the IR1, TR1, and TX1 and TX1 and TX8 groups (P<0.01). Under NANC conditions, spontaneous activity increased in TR1 and in both TX1 and TX8 (P<0.01) despite the lack of an increase in the frequency of contraction in TX1. Electrical field stimulation inhibited contractile activity at low frequencies, but under NANC conditions this inhibition persisted at higher frequencies. The calculated equieffective frequency (F100) that produced a response equal to baseline contractile activity was similar in all groups, but under NANC conditions was greater in TX1 (P<0.025). Functional alterations of NANC nerves are partly responsible for the increase in spontaneous activity in rat jejunal circular muscle strips after a limited ischemia/reperfusion injury, after selective disruption of enteric neural continuity (transection/reanastomosis), and after small bowel transplantation. These findings may provide important insight into graft dysfunction after small bowel transplantation in humans. Supported by United States Public Health Service grant DK 39337 from the National Institutes of Health and by the Mayo Foundation. |
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