Intestinal resection induces angiogenesis within adapting intestinal villi.
OBJECTIVE
Adaptive growth of the intestinal mucosa in response to massive gut loss is fundamental for autonomy from parenteral nutrition. Although angiogenesis is essential for cellular proliferation in other tissues, its relevance to intestinal adaptation is unknown. We tested the hypothesis that resection-induced adaptation is associated with new blood vessel growth.


METHODS
Male C57Bl/6 mice underwent either a 50% small bowel resection or a sham (transection and reanastomosis) operation. After 1, 3, or 7 days, capillary density within the intestinal villi was measured using confocal microscopy. A messenger RNA reverse-transcriptase polymerase chain reaction (RT-PCR) array was used to determine angiogenic gene expression during adaptation.


RESULTS
Mice that underwent small bowel resection had a significantly increased capillary density compared to sham-operated mice at postoperative day 7. This morphological alteration was preceded by significant alterations in 5 candidate genes at postoperative day 3.


CONCLUSIONS
New vessel blood growth is observed in the adapting intestine after massive small bowel loss. This response appears to follow rather than initiate the adaptive alterations in mucosal morphology that are characteristic of adaptation. A better understanding of this progress and the signaling factors involved may improve therapeutic options for children with short gut syndrome.
Martin
Colin A
CA
Division of Pediatric General and Thoracic Surgery, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
Perrone
Erin E
EE
Longshore
Shannon W
SW
Toste
Paul
P
Bitter
Kathryn
K
Nair
Rajalakshmi
R
Guo
Jun
J
Erwin
Christopher R
CR
Warner
Brad W
BW
D000222:Adaptation, Physiological; D000818:Animals; D004195:Disease Models, Animal; D007413:Intestinal Mucosa / Q000502:physiology*; D007421:Intestine, Small / Q000601:surgery*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018919:Neovascularization, Physiologic / Q000502:physiology*