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Updated: Mar 1, 2026

Ischemic Tissue Injury in the Dorsal Skinfold Chamber of the Mouse: A Skin Flap Model to Investigate Acute Persistent Ischemia
Published on: November 17, 2014
Inflammatory response associated with choke vessel remodeling in the extended perforator flap model
Liming Qing1, Pengfei Lei1, Juyu Tang1
1Department of Orthopaedics, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
Abstract:
Ischemic necrosis of the surgical flap is a common complication. The behavior of choke vessels has an important role in skin flap survival. However, the mechanism of choke vessel remodeling has remained elusive. The purpose of the present study was to investigate the possible association between inflammatory responses and choke vessel remodeling in the extended perforator flap model in rats. After flap elevation, the animals were randomly divided into three groups (n=6 in each) for tissue analysis at three, five or seven days after flap surgery. Six additional rats served as a control group (no flap elevation). Tissue samples were collected from the choke zone for histological, western blot and PCR analyses. Monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-α (TNF-α) as inflammatory cytokines were examined in the present study. Histopathological analysis showed that dilation of choke vessels and increased vessel wall thickness was obvious after flap elevation. It also showed edema, inflammation cell aggregation after the operation. Compared with the control group, the protein and mRNA expression levels of MCP-1 and TNF-α were significantly increased at days 3, 5 and 7 after flap elevation, while reaching a maximum at day 5. These findings indicated that inflammatory responses may have an important role in choke vessel remodeling. MCP-1 and TNF-α may be considered as potential targets for modulating the behavior of choke vessels.
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