Liu Yang, Hu Da-hai, Dong Mao-long, Wang Yun-chuan, Liu Jia-qi, Bai Li, Bai Xiao-zhi
Burns Center of PLA, Department of Burns and Cutaneous Surgery, Xijing Hospital, the Fourth Military Medical University, Xi'an 710032, China.
Zhonghua Shao Shang Za Zhi. 2011 Aug;27(4):255-9.
To observe the effect of vacuum sealing drainage (VSD) on the proliferation of Pseudomonas aeruginosa (PA) in infected wound, and to explore its possible mechanism.
Full-thickness skin wounds each with area of 1 cm x 1 cm were produced on the back of 40 C57 BL/6 mice, and then they were contaminated with wild type PA strains PAO1 marked with target gene of bacterial luciferase luxCDABE (PAO1-lux), they were dressed for 24 hours to reproduce PA infection model. Then mice were divided into experiment [E, with treatment of VSD (pressure value at -16.625 kPa)] and control (C, with treatment of conventional dressing change) groups according to the random number table, with 20 mice in each group. The fluorescence intensity of PAO1-lux and blood flow in wound was respectively measured by in vivo optical imaging system and laser Doppler perfusion imager before treatment and at post treatment hour (PTH) 24. The expression levels of IL-1beta and vascular endothelial growth factor (VEGF) mRNA in wound edge were determined by real-time fluorescence quantitative RT-PCR before treatment and at PTH 24. The specimens of wound edge tissue were collected for observation of pathological change at PTH 24. Data were processed with t test.
There were no obvious difference in fluorescence intensity of PAO1-lux and blood flow in wound between E and C groups before treatment (with t value respectively 0.03, 0.50, P values all above 0.05). The fluorescence intensity of PAOl-lux and blood flow in wound in E group at PTH 24 [(2.69 +/- 0.75) photons x s(-1) x cm(-2) x sr(-1) and (96 +/- 9) PU] was respectively lower and higher than that inC group [(5.18 +/- 0.96) photons x s(-1) cm x (-2) x sr(-1) and (70 +/- 11) PU, with t value respectively 3.54, 3.13, P values all below 0.05]. The expression levels of IL-1beta and VEGF mRNA in both groups before treatment were similar (with t value respectively 0.19, 0.07, P values all above 0.05). The expression levels of IL-1beta and VEGF mRNA in E group at PTH 24 was respectively 4.72 +/- 0.37, 2.68 +/- 0.39, all markedly higher than those in C group (2.24 +/- 0.50, 1.22 +/- 0.13, with t value respectively 6.90, 6.12, P values all equal to 0.00). The number of inflammatory cell infiltrating the wound edge in E group at PTH 24 was increased by nearly 77% as compared with that in C group.
Compared with conventional dressing change, VSD can reduce the amount of Pseudomonas aeruginosa in full-thickness skin defect wound at the early stage, it may be related with an increase in blood flow and number of inflammatory cells in wound tissue, promoting expression of IL-1beta and VEGF mRNA.
观察封闭式负压引流(VSD)对感染伤口铜绿假单胞菌(PA)增殖的影响,并探讨其可能机制。
在40只C57 BL/6小鼠背部制作面积为1 cm×1 cm的全层皮肤伤口,然后用标记有细菌荧光素酶luxCDABE靶基因的野生型PA菌株PAO1进行污染,包扎24小时以建立PA感染模型。然后根据随机数字表将小鼠分为实验组[E组,采用VSD治疗(压力值为-16.625 kPa)]和对照组[C组,采用传统换药治疗],每组20只。在治疗前及治疗后24小时(PTH 24),分别采用活体光学成像系统和激光多普勒血流成像仪测量伤口处PAO1-lux的荧光强度和血流情况。采用实时荧光定量RT-PCR法测定治疗前及PTH 24时伤口边缘白细胞介素-1β(IL-1β)和血管内皮生长因子(VEGF)mRNA的表达水平。在PTH 24时采集伤口边缘组织标本观察病理变化。数据采用t检验处理。
治疗前,E组和C组伤口处PAO1-lux的荧光强度和血流情况无明显差异(t值分别为0.03、0.50,P值均大于0.05)。E组在PTH 24时伤口处PAO1-lux的荧光强度[(2.69±0.75)光子·秒-1·厘米-2·球面度-1]低于C组[(5.18±0.96)光子·秒-1·厘米-2·球面度-1],血流情况[(96±9)PU]高于C组[(70±11)PU],t值分别为3.54、3.13,P值均小于0.05。两组治疗前IL-1β和VEGF mRNA的表达水平相似(t值分别为0.19、0.07,P值均大于0.05)。E组在PTH 24时IL-1β和VEGF mRNA的表达水平分别为4.72±0.37、2.68±0.39,均明显高于C组(2.24±0.50、1.22±0.13),t值分别为6.90、6.12,P值均等于0.00。与C组相比,E组在PTH 24时伤口边缘炎性细胞浸润数量增加了近77%。
与传统换药相比,VSD可在早期减少全层皮肤缺损伤口处铜绿假单胞菌的数量,其机制可能与增加伤口组织血流和炎性细胞数量、促进IL-1β和VEGF mRNA表达有关。