Fatma Tugba Güçlü Güvenç, Özlem Balci, Hilal Nakkas, Habibe Meltem Ozguner, Ismet Faruk Özgüner
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.
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.