供体来源纤维蛋白基质作为显微外科喉返神经修复辅助手段:一项实验性大鼠研究
Donor-Derived Fibrin Matrix as an Adjunct to Microsurgical Recurrent Laryngeal Nerve Repair: An Experimental Rat Study.
文献信息
| PMID | 42940082 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Alper Varman |
| 作者单位 | General Surgery Department, Faculty of Medicine, Necmettin Erbakan University, 42090 Konya, Türkiye. |
| 期刊 | Biomedicines |
| SCI 分区 | Q2 |
| IF | 4.7 |
| 研究类型 | 基础研究 · 基础/转化 |
| 所属专科 | 咽喉科 |
中文摘要
背景/目的: 喉返神经(RLN)横断可能导致持续性声带功能障碍,尽管进行了显微外科重建。生物支架可能支持神经愈合并保护靶肌肉。本研究评估了供体来源纤维蛋白基质作为大鼠原发性显微外科RLN修复辅助手段的作用。方法:27只雌性Wistar白化大鼠被分配到三组(每组n=9):RLN横断不修复组、原发性端端显微外科修复组,以及相同修复并补充供体来源纤维蛋白基质组。3个月后通过喉镜检查评估声带活动度。评估RLN损伤/修复部位的声带肌肉萎缩和组织病理学变化。结果:分别有0/9、2/9和4/9只动物观察到声带活动度,组间差异无统计学意义(p=0.116)。声带肌肉萎缩在各组间差异显著(p<0.001)。横断组所有动物均发生严重萎缩,原发性修复组有4/9发生严重萎缩,而纤维蛋白基质组未发生严重萎缩;该组7/9只动物无萎缩。炎症(p=0.003)、水肿(p=0.008)、束状结构紊乱(p<0.001)和异物反应(p<0.001)也观察到显著组间差异。轴突计数无显著差异(p=0.085)。结论:在显微外科RLN修复后,补充供体来源纤维蛋白基质与声带肌肉萎缩减少及更有利的组织病理学表现相关。尽管纤维蛋白基质组的声带活动度在数值上更高,但差异无统计学意义;因此,不能得出功能恢复有明确改善的结论。这些发现提示纤维蛋白基质补充可能具有结构性益处,值得在更大规模、采用更敏感功能评估的研究中进一步探讨。
英文摘要
Background/Objectives: Recurrent laryngeal nerve (RLN) transection may cause persistent vocal fold dysfunction despite microsurgical reconstruction. Biological scaffolds may support nerve healing and preserve target muscle. This study evaluated a donor-derived fibrin matrix as an adjunct to primary microsurgical RLN repair in rats. Methods: 27 female Wistar albino rats were assigned to three groups (n = 9 each): RLN transection without repair, primary end-to-end microsurgical repair, and identical repair supplemented with donor-derived fibrin matrix. Vocal fold mobility was assessed by laryngoscopy after 3 months. Vocal fold muscle atrophy and histopathological changes at the RLN injury/repair site were evaluated. Results: Vocal fold mobility was observed in 0/9, 2/9, and 4/9 animals, respectively, without a significant between-group difference (p = 0.116). Vocal fold muscle atrophy differed significantly among groups (p < 0.001). Severe atrophy occurred in all animals in the transection group and in 4/9 after primary repair, whereas no severe atrophy occurred in the fibrin matrix group; 7/9 animals in this group had no atrophy. Significant group differences were also observed for inflammation (p = 0.003), edema (p = 0.008), fascicular organization disorder (p < 0.001), and foreign-body reaction (p < 0.001). Axon counts did not differ significantly (p = 0.085). Conclusions: Donor-derived fibrin matrix supplementation was associated with reduced vocal fold muscle atrophy and more favorable histopathological findings after microsurgical RLN repair. Although vocal fold mobility was numerically higher in the fibrin matrix group, the difference was not statistically significant; therefore, no definitive improvement in functional recovery can be concluded. These findings suggest a potential structural benefit of fibrin matrix supplementation and warrant further investigation in larger studies with more sensitive functional assessments.