Egger B, Inglin R, Zeeh J, Dirsch O, Huang Y, Büchler M W
Department of Visceral and Transplantation Surgery, University of Berne, Berne, Switzerland.
Br J Surg. 2001 Jan;88(1):90-8. doi: 10.1046/j.1365-2168.2001.01617.x.
Human full-length keratinocyte growth factor (KGF) promotes healing of colon anastomoses in rats through mechanisms other than enhancement of collagen synthesis. Since insulin-like growth factor (IGF) I increases matrix synthesis, the aim of this study was to evaluate the effect of systemic truncated KGF (tKGF), IGF-I and combined tKGF-IGF-I administration on the healing of colonic anastomoses in rats.
Rats underwent laparotomy, division of the left colon, and sigmoidosigmoidostomy. tKGF (1 mg/kg), IGF-I (1 mg/kg), tKGF-IGF-I (both 1 mg/kg) or vehicle was administered intraperitoneally in four groups (n = 18 per group) 12 h before surgical intervention, and then once daily until killing (six animals per group; 2, 4 and 6 days after surgery). Bursting pressure measurements, histological evaluation, morphometric analysis, mucin and collagen staining, and 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry of the anastomotic site were undertaken.
Administration of tKGF, IGF-I and the combination of both growth factors significantly increased anastomotic bursting pressure at postoperative day 2 (63, 71 and 113 per cent respectively), day 4 (68, 83 and 80 per cent) and day 6 (48, 43 and 43 per cent) compared with the control group. No intergroup differences were found. Histological examination, mucin and BrdU staining, and measurement of colonic crypt depth indicated less inflammation, increased acidic mucin content, a higher crypt cell proliferation rate and thickened mucosal layer in the growth factor-treated animals than in controls. Enhanced collagen staining was observed only in IGF-treated animals.
tKGF and IGF-I markedly accelerate the healing of colonic anastomoses in rats. However, combined administration of the two growth factors does not show additional benefit. Both growth factors may be acting to accelerate host reparative processes as well as to enhance protection of the anastomotic wound bed.
人全长角质形成细胞生长因子（KGF）通过增强胶原蛋白合成以外的机制促进大鼠结肠吻合口愈合。由于胰岛素样生长因子（IGF）-I可增加基质合成，本研究旨在评估全身应用截短型KGF（tKGF）、IGF-I及联合应用tKGF-IGF-I对大鼠结肠吻合口愈合的影响。
大鼠行剖腹术、左半结肠离断及乙状结肠-乙状结肠吻合术。在手术干预前12小时，四组（每组n = 18）大鼠分别腹腔注射tKGF（1 mg/kg）、IGF-I（1 mg/kg）、tKGF-IGF-I（均为1 mg/kg）或赋形剂，然后每日一次直至处死（每组6只动物；术后2、4和6天）。对吻合口部位进行爆破压力测量、组织学评估、形态计量分析、黏蛋白和胶原蛋白染色以及5-溴-2'-脱氧尿苷（BrdU）免疫组化。
与对照组相比，tKGF、IGF-I及两种生长因子联合应用在术后第2天（分别为63%、71%和113%）、第4天（68%、83%和80%）和第6天（48%、43%和43%）显著增加了吻合口爆破压力。未发现组间差异。组织学检查、黏蛋白和BrdU染色以及结肠隐窝深度测量表明，与对照组相比，生长因子治疗组动物炎症较轻、酸性黏蛋白含量增加、隐窝细胞增殖率较高且黏膜层增厚。仅在IGF治疗组动物中观察到胶原蛋白染色增强。
tKGF和IGF-I显著加速大鼠结肠吻合口愈合。然而，联合应用这两种生长因子未显示出额外益处。两种生长因子可能都在加速宿主修复过程以及增强对吻合口创面床的保护方面发挥作用。
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