【摘要】：目的探討在呼吸機相關性肺損傷的大鼠模型中肺組織TLR-1、TLR-2表達的情況。 方法120只SPrague Dawley大鼠隨機分成對照組(A組,自主呼吸組)、正常通氣組(B組,VT=10ml/kg)、過度通氣潮氣量組(C組,VT=20ml/kg)及過度通氣大潮氣量組(D組,VT=40ml/kg),每組30只。各組按通氣時間(60min、120min和240min)再隨機分為3亞組,每亞組10只。所有大鼠均采用經口氣管插管,實驗組(B、C、D組)應用小型動物呼吸機予雙肺機械通氣,對照組(A組)在插管后保持自主呼吸。各組實驗結束后,頸總動脈放血處死大鼠,并取肺組織。光鏡下觀察肺組織的病理改變,利用RT-PCR檢測各組肺組織TLR-1mRNA、TLR-2mRNA表達和ELISA檢測各組肺組織中TLR-1、TLR-2的濃度。 結果①大鼠肺組織病理學變化：正常通氣組和對照組未見明顯肺損傷表現(xiàn)；C組在光鏡下可見少量肺間質水腫和炎癥細胞浸潤；D組可見肺組織點狀或者片狀出血,肺間隔增寬,肺間質明顯水腫,肺泡腔融合,大量炎性細胞積聚,部分肺組織有實變；②TLR-1、TLR-2及肺組織TLR-1mRNA、TLR-2mRNA的表達：B、C、D組與A組比較,TLR-1及TLR-1mRNA的表達差異無統(tǒng)計學意義(P0.05),B組與A組比較,TLR-2及TLR-2mRNA的表達差異性無統(tǒng)計學意義(P0.05),C、D組分別與A組比較,TLR-2的表達明顯高于對照組,差異有統(tǒng)計學意義(P0.05),D組亞組比較,通氣240min明顯高于通氣60min亞組,差異有統(tǒng)計學意義(P0.05)。 結論大潮氣量的機械通氣和長時間機械通氣會導致VILI,同時,可上調肺組織中TLR-2mRNA表達。
[Abstract]:Objective to investigate the expression of TLR-1,TLR-2 in lung tissue of ventilator-associated lung injury rats. Methods 120 SPrague Dawley rats were randomly divided into three groups: control group (group A, spontaneous breathing group), normal ventilation group (group B, VT=10ml/kg), hyperventilation tidal volume group (group C, VT=20ml/kg) and hyperventilation high tidal volume group (group D, VT=40ml/kg). There are 30 in each group. All groups were randomly divided into 3 subgroups according to ventilation time (60 min, 120 min and 240min), 10 rats in each subgroup. All rats were treated with tracheal intubation. The experimental group (B, C, D) was ventilated with small animal ventilator. The control group (group A) kept breathing autonomously after intubation. At the end of the experiment, the rats were killed by common carotid artery bleeding and lung tissue was obtained. The pathological changes of lung tissue were observed under light microscope. The expression of TLR-1mRNA,TLR-2mRNA in lung tissue was detected by RT-PCR and the concentration of TLR-1,TLR-2 in lung tissue was measured by ELISA. Results (1) pathological changes of rat lung: there was no obvious lung injury in normal ventilation group and control group, and a small amount of pulmonary interstitial edema and inflammatory cell infiltration were observed in group C under light microscope. In group D, punctate or lamellar hemorrhage, widening of pulmonary septum, obvious edema of pulmonary interstitial, fusion of alveolar cavity, accumulation of a large number of inflammatory cells and consolidation of some lung tissues were observed. 2the expression of TLR1, TLR2 and TLR-1mRNA,TLR-2mRNA in lung tissue: there was no significant difference in the expression of TLR-1 and TLR-1mRNA between group B, C, D and A (P0.05 compared with group A, P 0.05). There was no significant difference in the expression of TLR-2 and TLR-2mRNA (P0.05). Compared with group A, the expression of TLR-2 in group C, D was significantly higher than that in group A (P0.05). There was significant difference in expression of TLR-2 (P0.05) between group), D and group A (P0.05). Ventilation 240min was significantly higher than ventilation 60min subgroup, the difference was statistically significant (P0.05). Conclusion large tidal volume mechanical ventilation and long-term mechanical ventilation can lead to VILI, and up-regulate the expression of TLR-2mRNA in lung tissue.
【學位授予單位】：廣西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2013
【分類號】：R563

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