A Novel Preclinical Rat Model of Acute Compartment Syndrome

Abstract

Acute compartment syndrome (ACS) is common in trauma, challenging early diagnosis and treatment. An accurate ACS model is vital for its management. Most prior animal models have induced intrafascial hypertension by exogenous interventions, focusing on the study of secondary injury post-ACS formation. A novel rat model with spontaneous ACS formation after trauma was constructed, emphasizing early onset and development. The 300-mmHg pressure simulated by a blood pressure cuff was applied to rat hindlimbs for 3 h. A balloon catheter connected to a manometer was developed, and intracompartmental pressure (ICP) and blood perfusion were measured continuously for 2 h. H&E staining and serum index were detected at 0, 1-, 2-, 3-, and 8-h postinjury. The results showed injured hindlimbs swelled, with ICP rising continuously, reaching 30 mmHg in 35 min, peaking at 60–80 min before entering a plateau period, effectively reproducing ACS pressure evolution. The blood perfusion showed a three-step change, negatively correlating with ICP > 30 mmHg. Muscle tissues presented typical time-dependent pathological changes, with progressive myofibrillar rupture, inflammatory cell infiltration, and increases in serum IL-1β, TNF-α, CK, and BUN over time. This study successfully established a new preclinical ACS-like rat model. Compared with previous studies, the ICP in the hindlimbs in this study was spontaneously elevated after crush, leading to secondary injury. Furthermore, a new manometric catheter device was developed to enable continuous monitoring of ICP without repeated fluid injections. The constructed animal model is closer to the clinic, and it lays a solid foundation for ACS pathogenesis.