Chronic morpho-functional damage as a consequence of transient ischemia/reperfusion injury of the small bowel

Sergio Morini, Georg Elias, Melisa Brown, Vladimir Subbotin, Cristiana Rastellini, Luca Cicalese

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Introduction: The prevailing notion is that ischemia reperfusion injury of the small bowel induces transient changes that resolve within a few days postoccurrence. However, chronic injury has been described following a single ischemia reperfusion in the kidney. We proceeded to ascertain if a similar outcome is also witnessed in the small bowel. Materials and methods: ACI rats (n=32) underwent 1, 2 or 3 episodes of ischemia reperfusion by clamping the superior mesenteric artery for 45 minutes at 7-day intervals. Control groups included sham-operated (n=6) or nonoperated (n=5) rats. Morphology was examined at day ninety post-ischemia reperfusion and immunostaining was used to evaluate macrophage infiltration, microvascular distribution, and apoptosis. RT-PCR was used to evaluate expression of Inter-Cellular Adhesion Molecule-1 (ICAM-1), transforming growth factor-β (TGF-β), Insulin Growth Factor-I (IGF-1), and Insulin Growth Factor-I Receptor (IGF-R). Intestinal function was evaluated by D-xylose performed 24 hours and 4, 8, and 12 weeks after reperfusion. Results: Chronic morphologic changes were observed with degeneration of crypts, endothelial damage, matrix degeneration, and heightened lymphocyte degeneration within the Payer's patches. Major structural changes were characterized by villous atrophy from partial to total. The grade of histological injuries was significantly increased (P<0.001) after multiple ischemia reperfusion episodes. A higher number of apoptotic cells (P<0.001) and a prominent macrophage infiltration (P<0.05) was also witnessed. Altered expression of ICAM-1, TGF-β, and IGF-1 was observed. At 24 hours after ischemia reperfusion D-xylose absorption was diminished, returning to baseline values within 4 weeks and becoming abnormal again at 8 and 12 weeks (P<0.05). CONCLUSIONS: Unlike the prevailing conviction, these data demonstrate that transient ischemia reperfusion repeated injuries of the small bowel result in chronic intestinal damage.

Original languageEnglish (US)
Pages (from-to)277-286
Number of pages10
JournalHistology and Histopathology
Volume25
Issue number3
StatePublished - Mar 2010

Fingerprint

Reperfusion Injury
Reperfusion
Ischemia
Xylose
Transforming Growth Factors
Insulin-Like Growth Factor I
Inbred ACI Rats
Macrophages
Insulin
Superior Mesenteric Artery
Growth Factor Receptors
Wounds and Injuries
Constriction
Atrophy
Intercellular Signaling Peptides and Proteins
Cell Count
Lymphocytes
Apoptosis
Kidney
Polymerase Chain Reaction

Keywords

  • Chronic intestinal injury
  • Intestinal transient ischemia
  • Intestine
  • Small bowel
  • Transient ischemia/reperfusion

ASJC Scopus subject areas

  • Histology
  • Pathology and Forensic Medicine

Cite this

Chronic morpho-functional damage as a consequence of transient ischemia/reperfusion injury of the small bowel. / Morini, Sergio; Elias, Georg; Brown, Melisa; Subbotin, Vladimir; Rastellini, Cristiana; Cicalese, Luca.

In: Histology and Histopathology, Vol. 25, No. 3, 03.2010, p. 277-286.

Research output: Contribution to journalArticle

Morini, Sergio ; Elias, Georg ; Brown, Melisa ; Subbotin, Vladimir ; Rastellini, Cristiana ; Cicalese, Luca. / Chronic morpho-functional damage as a consequence of transient ischemia/reperfusion injury of the small bowel. In: Histology and Histopathology. 2010 ; Vol. 25, No. 3. pp. 277-286.
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AU - Morini, Sergio

AU - Elias, Georg

AU - Brown, Melisa

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AU - Rastellini, Cristiana

AU - Cicalese, Luca

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N2 - Introduction: The prevailing notion is that ischemia reperfusion injury of the small bowel induces transient changes that resolve within a few days postoccurrence. However, chronic injury has been described following a single ischemia reperfusion in the kidney. We proceeded to ascertain if a similar outcome is also witnessed in the small bowel. Materials and methods: ACI rats (n=32) underwent 1, 2 or 3 episodes of ischemia reperfusion by clamping the superior mesenteric artery for 45 minutes at 7-day intervals. Control groups included sham-operated (n=6) or nonoperated (n=5) rats. Morphology was examined at day ninety post-ischemia reperfusion and immunostaining was used to evaluate macrophage infiltration, microvascular distribution, and apoptosis. RT-PCR was used to evaluate expression of Inter-Cellular Adhesion Molecule-1 (ICAM-1), transforming growth factor-β (TGF-β), Insulin Growth Factor-I (IGF-1), and Insulin Growth Factor-I Receptor (IGF-R). Intestinal function was evaluated by D-xylose performed 24 hours and 4, 8, and 12 weeks after reperfusion. Results: Chronic morphologic changes were observed with degeneration of crypts, endothelial damage, matrix degeneration, and heightened lymphocyte degeneration within the Payer's patches. Major structural changes were characterized by villous atrophy from partial to total. The grade of histological injuries was significantly increased (P<0.001) after multiple ischemia reperfusion episodes. A higher number of apoptotic cells (P<0.001) and a prominent macrophage infiltration (P<0.05) was also witnessed. Altered expression of ICAM-1, TGF-β, and IGF-1 was observed. At 24 hours after ischemia reperfusion D-xylose absorption was diminished, returning to baseline values within 4 weeks and becoming abnormal again at 8 and 12 weeks (P<0.05). CONCLUSIONS: Unlike the prevailing conviction, these data demonstrate that transient ischemia reperfusion repeated injuries of the small bowel result in chronic intestinal damage.

AB - Introduction: The prevailing notion is that ischemia reperfusion injury of the small bowel induces transient changes that resolve within a few days postoccurrence. However, chronic injury has been described following a single ischemia reperfusion in the kidney. We proceeded to ascertain if a similar outcome is also witnessed in the small bowel. Materials and methods: ACI rats (n=32) underwent 1, 2 or 3 episodes of ischemia reperfusion by clamping the superior mesenteric artery for 45 minutes at 7-day intervals. Control groups included sham-operated (n=6) or nonoperated (n=5) rats. Morphology was examined at day ninety post-ischemia reperfusion and immunostaining was used to evaluate macrophage infiltration, microvascular distribution, and apoptosis. RT-PCR was used to evaluate expression of Inter-Cellular Adhesion Molecule-1 (ICAM-1), transforming growth factor-β (TGF-β), Insulin Growth Factor-I (IGF-1), and Insulin Growth Factor-I Receptor (IGF-R). Intestinal function was evaluated by D-xylose performed 24 hours and 4, 8, and 12 weeks after reperfusion. Results: Chronic morphologic changes were observed with degeneration of crypts, endothelial damage, matrix degeneration, and heightened lymphocyte degeneration within the Payer's patches. Major structural changes were characterized by villous atrophy from partial to total. The grade of histological injuries was significantly increased (P<0.001) after multiple ischemia reperfusion episodes. A higher number of apoptotic cells (P<0.001) and a prominent macrophage infiltration (P<0.05) was also witnessed. Altered expression of ICAM-1, TGF-β, and IGF-1 was observed. At 24 hours after ischemia reperfusion D-xylose absorption was diminished, returning to baseline values within 4 weeks and becoming abnormal again at 8 and 12 weeks (P<0.05). CONCLUSIONS: Unlike the prevailing conviction, these data demonstrate that transient ischemia reperfusion repeated injuries of the small bowel result in chronic intestinal damage.

KW - Chronic intestinal injury

KW - Intestinal transient ischemia

KW - Intestine

KW - Small bowel

KW - Transient ischemia/reperfusion

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