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Updated: Aug 8, 2026
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Therapeutic Effects of Carvedilol on Intestinal Mucosa in Intestinal Ischemia Reperfusion Injury Model; An
Fatma Tugba Güçlü Güvenç1, Özlem Balci1, Hilal Nakkas2
1Department of Pediatric Surgery, Dr. Sami Ulus Maternity and Children's Health and Diseases Training and Research Hospital, University of Health Sciences, Ankara, Turkey.
Background:
Intestinal ischemia-reperfusion (I/R) injury is a critical clinical condition associated with high morbidity and mortality, with acute mesenteric ischemia carrying mortality rates of 60%-80%. Carvedilol, a third-generation β-blocker with known antioxidant properties, has demonstrated protective effects against I/R injury in various organs. This study aimed to investigate the effects of carvedilol on intestinal I/R injury in an experimental rat model, with assessment of oxidative stress parameters and histopathological damage.
Materials And Methods:
Thirty-two male Wistar albino rats were randomly divided into four groups (n = 8 each): sham, sham + carvedilol (2 mg/kg IP), I/R (30 min of superior mesenteric artery occlusion followed by reperfusion), and I/R + carvedilol (I/R plus 2 mg/kg carvedilol IP immediately after reperfusion). At 48 h postprocedure, blood samples were collected for biochemical analysis, including total antioxidant status (TAS), total oxidant status (TOS), and thiol/disulfide homeostasis parameters (sulfhydryl [SH], total thiol [TT], and disulfide bonds). Intestinal tissue samples were evaluated histopathologically using the Chiu scoring system.
Results:
Carvedilol significantly reduced intestinal mucosal damage, with the I/R + carvedilol group showing markedly lower Chiu scores compared to the untreated I/R group (median 2.0 vs. 4.0, P < 0.001). Biochemically, the I/R group exhibited significantly lower SH and TT levels than sham controls (P = 0.003 and P = 0.006, respectively), indicating oxidative stress. Carvedilol treatment preserved thiol status, with the I/R + carvedilol group demonstrating significantly higher SH levels than the untreated I/R group (P = 0.002). No significant differences were observed in TAS, TOS, or glutathione levels between the groups.
Conclusion:
Postreperfusion administration of carvedilol significantly attenuated intestinal I/R injury, as evidenced by reduced histopathological damage scores and preserved thiol/disulfide homeostasis. These findings suggest that carvedilol's antioxidant properties may offer therapeutic potential in intestinal I/R injury. To our knowledge, this is the first study evaluating carvedilol in this context, warranting further investigation with different dosing regimens and timepoints.
