Electrical field stimulation promotes anastomotic healing in poorly perfused rat colon
Introduction Hypoperfusion of the bowel is a risk factor for anastomotic failure. Electrical field stimulation has been shown to improve repair in ischemic tissue, but its influence in hypoperfused colon has not been investigated. The hypothesis of this experimental animal study was that electrical...
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Veröffentlicht in: | International journal of colorectal disease 2011-03, Vol.26 (3), p.339-344 |
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Sprache: | eng |
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Zusammenfassung: | Introduction Hypoperfusion of the bowel is a risk factor for anastomotic failure. Electrical field stimulation has been shown to improve repair in ischemic tissue, but its influence in hypoperfused colon has not been investigated. The hypothesis of this experimental animal study was that electrical field stimulation improves anastomotic healing in ischemic bowel. Materials and methods Thirty rats were divided evenly into three groups: control, ischemia/placebo, and ischemia/test group. Ischemia was induced by ligation of the arterial supply to the proximal colon. The watershed area was identified and transected. Field stimulation was achieved by application of negatively charged diethylaminoethyl Sephadex beads in methylcellulose gel to the colonic epithelium prior to anastomosis. The placebo group had methylcellulose gel only applied and control animals had anastomosis only. Anastomotic strength was measured using anastomotic bursting pressure and hydroxyproline content. Systemic effect was investigated via interleukin-6 and vascular endothelial growth factor assay. Results The ischemia/electrical field stimulation (EFS) group had significantly increased bursting pressure and hydroxyproline content in comparison with the placebo group (P < 0.001). Serum cytokine levels were unaffected. Conclusion Negatively charged EFS improves anastomotic healing in hypoperfused colon without induction of systemic cytokines and has potential as a local treatment in high-risk bowel anastomosis. |
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ISSN: | 0179-1958 1432-1262 |
DOI: | 10.1007/s00384-010-1053-z |