Robson Martin C, Dubay Derek A, Wang Xue, Franz Michael G
Institute for Tissue Regeneration, Repair, and Rehabilitation, Department of Veterans Affairs, Bay Pines, and Department of Surgery, University of South Florida, Tampa, Florida, USA.
Wound Repair Regen. 2004 Jan-Feb;12(1):38-43. doi: 10.1111/j.1067-1927.2004.012109.x.
Cytokine growth factor treatment of chronic wounds has met with mixed results. The chronic wound presents a hostile environment to peptides such as growth factors. Cytokine growth factors have not been studied extensively in acute wounds. However, incisional hernias are a major example of acute wound failure that has not been solved by various mechanical approaches. A biological approach to acute wound failure by use of cytokine growth factors may offer a new strategy. A rodent incisional hernia model was used. Seventy-six rats underwent 3-cm midline celiotomies and were closed with fine, fast-absorbing sutures to induce intentional acute wound failure. Group 1 received no other treatment. The midline fascia in Groups 2-10 was infiltrated with 100 microl of vehicle alone or vehicle containing various test cytokine growth factors. Necropsy was performed on postoperative day 28 and the wounds were examined for herniation. Incisional hernias developed in 83 percent (13/16) of untreated incisional and 88 percent (7/8) and 83 percent (5/6) of the two vehicle-treated incisions (PBS and carboxymethylcellulose). Hernia incidences were decreased by priming of the fascial incision with transforming growth factor-beta(2) (12%, 1/8), basic fibroblast growth factor (25%, 2/8) and interleukin-1 beta (50%, 3/6) (p < 0.05). Aqueous platelet-derived growth factor, becaplermin, insulin-like growth factor, and granulocyte macrophage-colony stimulating factor did not significantly decrease the incidence of acute wound failure (p > 0.05). A biological approach to acute wound failure as measured by incisional hernia formation can be useful in reducing the incidence of this complication. Transforming growth factor-beta(2), basic fibroblast growth factor, and interleukin 1 beta all eliminated or significantly reduced the development of incisional hernias in the rat model.
细胞因子生长因子治疗慢性伤口的效果不一。慢性伤口对生长因子等肽类物质而言是一个不利的环境。细胞因子生长因子在急性伤口方面尚未得到广泛研究。然而,切口疝是急性伤口愈合失败的一个主要例子,各种机械方法都未能解决这一问题。利用细胞因子生长因子对急性伤口愈合失败采取生物学方法可能会提供一种新策略。采用了一种啮齿动物切口疝模型。76只大鼠接受了3厘米的中线剖腹术,并用精细、快速吸收的缝线缝合,以诱发故意的急性伤口愈合失败。第1组未接受其他治疗。第2 - 10组的中线筋膜分别注射100微升单独的赋形剂或含有各种测试细胞因子生长因子的赋形剂。在术后第28天进行尸检,并检查伤口是否出现疝。未治疗的切口中有83%(13/16)出现切口疝,两种赋形剂治疗的切口(PBS和羧甲基纤维素)中分别有88%(7/8)和83%(5/6)出现切口疝。用转化生长因子-β(2)(12%,1/8)、碱性成纤维细胞生长因子(25%,2/8)和白细胞介素-1β(50%,3/6)预处理筋膜切口可降低疝的发生率(p < 0.05)。水性血小板衍生生长因子、贝卡普勒明、胰岛素样生长因子和粒细胞巨噬细胞集落刺激因子并未显著降低急性伤口愈合失败的发生率(p > 0.05)。以切口疝形成来衡量,对急性伤口愈合失败采取生物学方法有助于降低这种并发症的发生率。转化生长因子-β(2)、碱性成纤维细胞生长因子和白细胞介素1β均消除或显著减少了大鼠模型中切口疝的发生。