目的观察半导体激光局部照射SD大鼠缺血皮瓣创面愈合时组织中炎症反应因子细胞间黏附分子－1（intercellular cell adhesion molecule-1，ICAM-1）和单核细胞趋化蛋白－1（monocyte chemotactic protein-1，MCP-1）的表达，探讨其促进缺血皮瓣愈合的机制。方法在20只雄性SD大鼠背部两侧对称各制备2个皮瓣，蒂位于尾侧，长6 cm，宽1 cm，2个皮瓣间距离2 cm。实验侧（实验组）皮瓣术后行半导体激光照射，每天1次，连续照射数天直至取材，同时遮挡对照侧（对照组）。采用自身对照法比较实验组和对照组的创面愈合情况和皮瓣存活面积，分别于术后4、7、10、14 d取皮瓣中段组织进行病理学染色，分析制备的大鼠皮瓣血管形成情况和炎症反应因子ICAM-1和MCP-1的表达。结果皮瓣远端发生明显的缺血坏死。术后7 d，实验组和对照组的皮瓣存活率分别为（84．6±10．8）％和（79．8±11．3）％，实验组皮瓣存活率明显高于对照组（n＝5，t＝7．299，P＝0.002）。术后4、7、10、14 d实验组微血管密度分别为（74．160±25．968）、（115．937±17．827）、（87.330±21．383）、（69．644±12．126）个／mm2，均明显高于对照组（33．460±8．310）个／mm2（ t ＝3．089， P ＝0．037）、（36．685±7．693）个／mm2（t＝11．741，P＝0．000）、（43．474±7．400）个／mm2（t＝4．185，P＝0．014）、37．104±8．721（t＝5．218， P＝0．006）。术后4 d实验组炎症因子ICAM-1的表达量0．063±0．015明显高于对照组0．045±0．017（t＝8．430，P＝0．001）；术后7 d实验组炎症因子ICAM-1和MCP-1的表达量分别为0．022±0．008、0．041±0．008，均明显低于对照组0．042±0.015（t＝4．309，P＝0.013）、0．065±0．007（t＝6．731，P＝0.003）。结论半导体激光局部照射SD大鼠缺血皮瓣能调节创面愈合时炎症因子ICAM-1和MCP-1的表达，是促进缺血皮瓣愈合的重要机制之一。%Objective To study the mechanism of semiconductor laser local irradiation in promoting the healing of ischemic skin flap in Sprague-Dawley(SD) rats by investigating the expression of inflammatory factors of intercellular cell adhesion molecule -1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1). Methods Two symmetrical skin flaps were prepared at the back of a male SD rat with the pedicles located on the tail .Each flap was 6 cm in length and 1 cm in width, and the distance between the two flaps was 2 cm.One flap was treated with semiconductor laser local irradiation ( once daily until specimen collection ) and the other side was the control side .The self-control method was used to compare the differences between the two flaps .The survival area of flap , the vascular formation and the expressions of inflammation related molecules ICAM-1 and MCP-1 were detected respectively on the postoperative 4, 7, 10, and 14 d. Results The distal end of the skin flaps had obvious ischemic necrosis .The survival rate of flap and the microvascular density in the experimental group were significantly higher than those in the control group after the operation .On the 7th day, the survival rates of flaps in the experimental group and the control group were (84.6 ±10.8)%and (79.8 ±11.3)%, respectively.On the 4th, 7th, 10th, and 14th days, the microvessel densities ( per mm2 ) of the experimental group (74.160 ± 25.968, 115.937 ±17.827, 87.330 ±21.383, and 69.644 ±12.126) were significantly higher than those of the control group (33.460 ±8.310, t=3.089, P=0.037; 36.685 ±7.693, t =11.741, P=0.000; 43.474 ±7.400, t =4.185, P=0.014;37.104 ±8.721, t =5.218, P =0.006).On the 4th day after operation, the expression of ICAM-1 in the experimental group (0.063 ±0.015) was significantly higher than that in the control group (0.045 ±0.017, t=8.430, P=0.001), while on the 7th day after operation, the expressions of inflammatory cytokines of ICAM-1 and MCP-1 in the experimental group (0.022 ±0.008 and 0.041 ±0.008) were significantly lower than those in the control group (0.042 ±0.015, t=4.309, P=0.013;0.065 ±0.007, t=6.731, P=0.003). Conclusions The expression of inflammatory factors of MCP-1 and ICAM-1 during the healing of ischemic skin flap in SD rats can be regulated by semiconductor laser irradiation .This is an important mechanism to promote the healing of ischemic skin flap .
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