Effect of Intra-arterial Bemiparin Sodium on Intestinal Ischemia-Reperfusion Injury: Animal Model

Acute mesenteric ischemia is characterized by impaired intestinal perfusion and high mortality. Reperfusion injury contributes to morbidity through oxidative stress, inflammation, and endothelial dysfunction. This study investigates the protective effect of bemiparin sodium, a low-molecular-weight heparin with anti-inflammatory properties, in intestinal ischemia-reperfusion injury.

Thirty-five female Wistar albino rats (250-300 g) were divided into five groups (n = 7 each). In group 1, the superior mesenteric artery was isolated but not clamped. Groups two and three underwent superior mesenteric artery clamping for 30 and 60 min, respectively, followed by 120 min reperfusion. Groups four and five underwent identical procedures with intra-arterial administration of 70 IU/kg bemiparin sodium before reperfusion. Terminal ileum and jejunum tissue samples and intracardiac blood were collected. Mucosal damage was assessed by Chiu/Park grading, and systemic effects were evaluated through biochemical analysis (urea, creatinine, potassium, albumin, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and C-reactive protein).

In jejunal tissue, statistically significant differences in Chiu/Park grades were observed among groups (P < 0.05). Treated groups showed reduced injury scores (group four mean ± standard deviation: 1.71 ± 1.11) compared with untreated (group 2: 3.14 ± 2.04). In terminal ileum, trends toward improvement were observed, but did not reach statistical significance (P = 0.065). Biochemical markers (alanine aminotransferase, aspartate aminotransferase, and C-reactive protein) were significantly lower in treated groups.

Based on our findings in this rat model, intra-arterial bemiparin sodium may exert a protective effect against ischemia-reperfusion injury. Further studies are required to confirm its translational potential.