中华烧伤杂志
中華燒傷雜誌
중화소상잡지
16
2011年
4期
255-259
,共5页
刘洋%胡大海%董茂龙%王耘川%刘佳琦%白丽%白晓智
劉洋%鬍大海%董茂龍%王耘川%劉佳琦%白麗%白曉智
류양%호대해%동무룡%왕운천%류가기%백려%백효지
负压伤口疗法%假单胞菌,铜绿%感染%活体成像
負壓傷口療法%假單胞菌,銅綠%感染%活體成像
부압상구요법%가단포균,동록%감염%활체성상
Negative-pressure wound therapy%Pseudomonas aeruginosa%Infection%In vivo optical imaging system
目的 观察VSD对感染创面中铜绿假单胞菌生长的影响，并探讨其可能机制。 方法 选取健康成年雄性C57BL/6小鼠40只，按照随机数字表法分为对照组和治疗组，每组20只。无菌条件下切除各小鼠背部1 cm×1 cm的全层皮肤，将细菌荧光素酶目的基因luxCDABE标记的野生型铜绿假单胞菌菌株PAO1 -lux涂抹于创面，包扎创面24 h，制成铜绿假单胞菌感染小鼠模型。治疗组小鼠创面行VSD治疗（负压为-16.625 kPa），对照组创面常规换药。分别于治疗前和治疗24 h时，用小动物活体成像系统检测2组小鼠创面PAO1-lux荧光强度，激光多普勒血流成像仪检测创面血流量，以实时荧光定量RT-PCR检测创缘组织IL-1β、血管内皮生长因子(VEGF)的mRNA表达水平。观察治疗24 h时2组小鼠创缘组织病理学特点。对实验数据行t检验。 结果(1)治疗前，治疗组小鼠创面PAO1 -lux荧光强度与对照组相近(t=0.03,P=0.98)；治疗24 h时，治疗组的荧光强度为(2.69±0.75)光子·秒-1·厘米-2·单位角度-1(photons· s-1- cm-2·sr-1)，明显低于对照组的(5.18±0.96)photons·s-1·cm-2·sr-1，t =3.54，P=0.02。(2)治疗前，治疗组小鼠创面血流量与对照组相似(t =0.50，P=0.64)；治疗24 h时，治疗组创面血流量为(96±9)灌注单位，明显高于对照组的(70±11)灌注单位，t=3.13，P=0.04。(3)治疗前，2组小鼠创缘皮肤组织中IL-1β、VEGF mRNA表达水平接近（t=0.19，P=0.86；t=0.07，P=0.95）；治疗24h时，治疗组IL-1β、VEGF mRNA表达水平分别为4.72±0.37、2.68±0.39，均明显高于对照组的2.24±0.50、1.22±0.13，t值分别为6.90、6.12，P值均为0.00。(4)治疗24 h时，治疗组创缘皮肤组织内炎性细胞浸润数量较对照组增加约77％。 结论 与常规换药相比，VSD治疗在小鼠全层皮肤缺损早期即能明显降低创面铜绿假单胞菌含量。其机制可能与增加创面局部血流量、提高创面组织炎性细胞数量、促进IL-1β和VEGF的mRNA表达有关。
目的 觀察VSD對感染創麵中銅綠假單胞菌生長的影響，併探討其可能機製。 方法 選取健康成年雄性C57BL/6小鼠40隻，按照隨機數字錶法分為對照組和治療組，每組20隻。無菌條件下切除各小鼠揹部1 cm×1 cm的全層皮膚，將細菌熒光素酶目的基因luxCDABE標記的野生型銅綠假單胞菌菌株PAO1 -lux塗抹于創麵，包扎創麵24 h，製成銅綠假單胞菌感染小鼠模型。治療組小鼠創麵行VSD治療（負壓為-16.625 kPa），對照組創麵常規換藥。分彆于治療前和治療24 h時，用小動物活體成像繫統檢測2組小鼠創麵PAO1-lux熒光彊度，激光多普勒血流成像儀檢測創麵血流量，以實時熒光定量RT-PCR檢測創緣組織IL-1β、血管內皮生長因子(VEGF)的mRNA錶達水平。觀察治療24 h時2組小鼠創緣組織病理學特點。對實驗數據行t檢驗。 結果(1)治療前，治療組小鼠創麵PAO1 -lux熒光彊度與對照組相近(t=0.03,P=0.98)；治療24 h時，治療組的熒光彊度為(2.69±0.75)光子·秒-1·釐米-2·單位角度-1(photons· s-1- cm-2·sr-1)，明顯低于對照組的(5.18±0.96)photons·s-1·cm-2·sr-1，t =3.54，P=0.02。(2)治療前，治療組小鼠創麵血流量與對照組相似(t =0.50，P=0.64)；治療24 h時，治療組創麵血流量為(96±9)灌註單位，明顯高于對照組的(70±11)灌註單位，t=3.13，P=0.04。(3)治療前，2組小鼠創緣皮膚組織中IL-1β、VEGF mRNA錶達水平接近（t=0.19，P=0.86；t=0.07，P=0.95）；治療24h時，治療組IL-1β、VEGF mRNA錶達水平分彆為4.72±0.37、2.68±0.39，均明顯高于對照組的2.24±0.50、1.22±0.13，t值分彆為6.90、6.12，P值均為0.00。(4)治療24 h時，治療組創緣皮膚組織內炎性細胞浸潤數量較對照組增加約77％。 結論 與常規換藥相比，VSD治療在小鼠全層皮膚缺損早期即能明顯降低創麵銅綠假單胞菌含量。其機製可能與增加創麵跼部血流量、提高創麵組織炎性細胞數量、促進IL-1β和VEGF的mRNA錶達有關。
목적 관찰VSD대감염창면중동록가단포균생장적영향，병탐토기가능궤제。 방법 선취건강성년웅성C57BL/6소서40지，안조수궤수자표법분위대조조화치료조，매조20지。무균조건하절제각소서배부1 cm×1 cm적전층피부，장세균형광소매목적기인luxCDABE표기적야생형동록가단포균균주PAO1 -lux도말우창면，포찰창면24 h，제성동록가단포균감염소서모형。치료조소서창면행VSD치료（부압위-16.625 kPa），대조조창면상규환약。분별우치료전화치료24 h시，용소동물활체성상계통검측2조소서창면PAO1-lux형광강도，격광다보륵혈류성상의검측창면혈류량，이실시형광정량RT-PCR검측창연조직IL-1β、혈관내피생장인자(VEGF)적mRNA표체수평。관찰치료24 h시2조소서창연조직병이학특점。대실험수거행t검험。 결과(1)치료전，치료조소서창면PAO1 -lux형광강도여대조조상근(t=0.03,P=0.98)；치료24 h시，치료조적형광강도위(2.69±0.75)광자·초-1·전미-2·단위각도-1(photons· s-1- cm-2·sr-1)，명현저우대조조적(5.18±0.96)photons·s-1·cm-2·sr-1，t =3.54，P=0.02。(2)치료전，치료조소서창면혈류량여대조조상사(t =0.50，P=0.64)；치료24 h시，치료조창면혈류량위(96±9)관주단위，명현고우대조조적(70±11)관주단위，t=3.13，P=0.04。(3)치료전，2조소서창연피부조직중IL-1β、VEGF mRNA표체수평접근（t=0.19，P=0.86；t=0.07，P=0.95）；치료24h시，치료조IL-1β、VEGF mRNA표체수평분별위4.72±0.37、2.68±0.39，균명현고우대조조적2.24±0.50、1.22±0.13，t치분별위6.90、6.12，P치균위0.00。(4)치료24 h시，치료조창연피부조직내염성세포침윤수량교대조조증가약77％。 결론 여상규환약상비，VSD치료재소서전층피부결손조기즉능명현강저창면동록가단포균함량。기궤제가능여증가창면국부혈류량、제고창면조직염성세포수량、촉진IL-1β화VEGF적mRNA표체유관。
Objective 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. Methods Full-thickness skin wounds each with area of 1 cm × 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-1β 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. Results 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 PAO1-lux and blood flow in wound in E group at PTH 24 [(2.69 ±0.75) photons · s-1 · cm-2 · sr-1and (96 ±9) PU] was respectively lower and higher than that in C group [(5.18 ±0.96) photons · s-1 · cm-2 · 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-1 β 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-1β 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. Conclusions 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-1β and VEGF mRNA.
