Effect of Hyperbaric Oxygen Therapy in Reducing Intestinal Edema After Traumatic Liver Injury with Abdominal Packing: An Experimental Animal Study

Background: Traumatic liver injury in severe trauma and temporary abdominal closure can lead to postoperative intestinal edema and inflammation. Hyperbaric oxygen therapy (HBOT) may mitigate these effects by modulating inflammatory pathways. This study investigated the effects of HBOT on mucosal preservation, with villus height and the villus-to-crypt (V/C) ratio as primary outcomes and mechanistic analyses of the NLRP3/caspase-1 pathway. Methods: Twenty male Sprague–Dawley rats (aged 7 weeks, weighing 260–300 g) were randomly assigned to HBOT (n = 10) or non-HBOT groups (n = 10) and underwent midline laparotomy (3–5 cm) with 50% left lateral lobe liver resection. After 4 min, the liver was packed with 2 × 2 cm aseptic gauze and the abdomen was temporarily sutured. After 24 h, the small intestine was isolated and flushed with phosphate-buffered saline. The primary outcomes were villus height and the V/C ratio, measured in the proximal jejunum. Secondary outcomes included villus width, crypt depth, villous surface area, and the Dvorak histological injury grade. Additional analyses included NLRP3, AIM2, pro-caspase-1, cleaved caspase-1, IL-1β, and IL-18 expression in bowel tissue (Western blot); plasma IL-1β and IL-18 (ELISA); and peripheral blood mononuclear cell catalase activity, cell viability (CCK-8), and LDH release. Results: The HBOT group demonstrated greater villus height compared with the non-HBOT group (347.68 ± 42.48 μm vs. 290.43 ± 43.47 μm; p = 0.008), corresponding to a 19.7% increase. The V/C ratio was significantly higher in the HBOT group (2.56 ± 0.31 vs. 2.12 ± 0.23; p = 0.002). Villus width was significantly reduced in the HBOT group (64.65 ± 4.24 μm vs. 73.93 ± 9.49 μm; p = 0.015). Pathological findings indicated that the HBOT group showed attenuated lamina propria edema and separation. In the intestinal tissue samples, NLRP3 expression was significantly lower in the HBOT group (0.09 [0.09, 0.12] vs. 1.00 [0.92, 1.06]; p < 0.001), and AIM2, IL-1β, IL-18, and cleaved caspase-1 followed similar trends. Conclusions: HBOT preserved intestinal villus structure after traumatic liver injury, as evidenced by greater villus height and a higher villus-to-crypt ratio. At the molecular level, HBOT suppressed NLRP3, AIM2, and cleaved caspase-1 protein expression in bowel tissue and reduced IL-1β and IL-18 protein levels. By limiting inflammasome activation and interstitial edema, HBOT may help preserve intestinal structural integrity after damage-control surgery.