Department of Surgery, University of Michigan, Ann Arbor, MI 48109, USA.
Ann Surg. 2013 Jan;257(1):142-9. doi: 10.1097/SLA.0b013e31825ffd02.
To determine whether primary or mesh herniorrhaphy reverses abdominal wall atrophy and fibrosis associated with hernia formation.
We previously demonstrated that hernia formation is associated with abdominal wall atrophy and fibrosis after 5 weeks in an animal model.
A rat model of chronic incisional hernia was used. Groups consisted of uninjured control (UC, n = 8), sham repair (SR, n = 8), unrepaired hernia (UR, n = 8), and 2 repair groups: primary repair (PR, n = 8) or tension-free polypropylene mesh repair (MR, n = 8) hernia repair on postoperative day (POD) 35. All rats were killed on POD 70. Intact abdominal wall strips were cut perpendicular to the wound for tensiometric analysis. Internal oblique muscles were harvested for fiber type and size determination.
No hernia recurrences occurred after PR or MR. Unrepaired abdominal walls significantly demonstrated greater stiffness, increased breaking and tensile strengths, yield load and yield energy, a shift to increased type IIa muscle fibers than SR (15.9% vs 9.13%; P < 0.001), and smaller fiber cross-sectional area (CSA, 1792 vs 2669 μm(2); P < 0.001). PR failed to reverse any mechanical changes but partially restored type IIa fiber (12.9% vs 9.13% SR; P < 0.001 vs 15.9% UR; P < 0.01) and CSA (2354 vs 2669 μm(2) SR; P < 0.001 vs 1792 μm(2) UR; P < 0.001). Mesh-repaired abdominal walls demonstrated a trend toward an intermediate mechanical phenotype but fully restored type IIa muscle fiber (9.19% vs 9.13% SR; P > 0.05 vs 15.9% UR; P < 0.001) and nearly restored CSA (2530 vs 2669 μm(2) SR; P < 0.05 vs 1792 μm(2) UR; P < 0.001).
Mesh herniorrhaphy more completely reverses atrophic abdominal wall changes than primary herniorrhaphy, despite failing to restore normal anatomic muscle position. Techniques for hernia repair and mesh design should take into account abdominal wall muscle length and tension relationships and total abdominal wall compliance.
确定原发性或网片修补术是否能逆转与疝形成相关的腹壁萎缩和纤维化。
我们之前的研究表明，在动物模型中，疝形成 5 周后与腹壁萎缩和纤维化有关。
采用慢性切口疝大鼠模型。实验组包括未受伤对照组（UC，n=8）、假手术组（SR，n=8）、未修复疝组（UR，n=8）和 2 个修复组：原发性修复（PR，n=8）或无张力聚丙烯网片修补术（MR，n=8），于术后第 35 天进行疝修补术。所有大鼠均于术后第 70 天处死。垂直于切口切开完整腹壁条进行张力分析。采集内斜肌进行纤维类型和大小测定。
PR 或 MR 后无疝复发。与 SR 相比，未修复腹壁的硬度显著增加，断裂强度、拉伸强度、屈服载荷和屈服能量增加，Ⅱa 型肌纤维比例增加（15.9%比 9.13%；P<0.001），纤维横截面积（CSA）减小（1792 μm2比 2669 μm2；P<0.001）。PR 未能逆转任何力学变化，但部分恢复了Ⅱa 型纤维（12.9%比 9.13% SR；P<0.001 比 15.9% UR；P<0.01）和 CSA（2354 μm2比 2669 μm2 SR；P<0.001 比 1792 μm2 UR；P<0.001）。网片修补的腹壁表现出一种中间力学表型，但完全恢复了Ⅱa 型肌纤维（9.19%比 9.13% SR；P>0.05 比 15.9% UR；P<0.001），并几乎恢复了 CSA（2530 μm2比 2669 μm2 SR；P<0.05 比 1792 μm2 UR；P<0.001）。
尽管未能恢复正常的解剖肌肉位置，但网片疝修补术比原发性疝修补术更能完全逆转腹壁萎缩性变化。疝修补术和网片设计技术应考虑腹壁肌肉长度和张力关系以及整个腹壁顺应性。
