Abdominal Wall Repair Is Delayed during Hepatic Regeneration

Abstract

Background. Abdominal wall wound failure remains a common surgical problem. The signals that activate normal fibroplastic repair versus regeneration pathways are unknown. Transforming growth factor β levels rise during incisional healing but fall during hepatic regeneration. Changes in the injured host cytokine milieu may therefore differentially effect abdominal wall repair versus hepatic regeneration.Materials and methods. Forty-eight rats were divided into four groups (n = 12). Groups 1–3 underwent sham celiotomy, 70% hepatectomy, or 80% enterectomy with anastamosis. Incisions from Group 4 were treated with either 1 μg of transforming growth factor β2 (TGF-β2) or vehicle following hepatectomy. Isolated fascial and dermal incisions were harvested and tested for breaking strength on POD 7. Serum (TGF-β2) and hepatocyte growth factor (HGF) levels were measured by ELISA.Results. Recovery of incisional wound breaking strength was delayed following hepatectomy but not enterectomy (P < 0.002). The inhibitory effect was observed in both the fascia and the dermis of the abdominal wall. TGF-β2 levels were depressed in hepatectomy animals on POD 7, while at the same time HGF levels were elevated. Exogenous TGF-β2 shifted the healing trajectory of deficient wounds back toward a control pattern.Conclusion. Abdominal wall fascial and dermal healing is delayed during hepatic regeneration. Elevated HGF and depressed TGF-β2 suggest a host mechanism that prioritizes hepatic parenchymal regeneration over fibroplastic repair (scar). Observations such as these are needed as therapeutic wound healing enters the clinical realm.