机构地区:[1]南昌大学第一附属医院麻醉科,南昌330006 [2]江西省人民医院肿瘤科,南昌330006
出 处:《中南大学学报(医学版)》2018年第11期1177-1181,共5页Journal of Central South University :Medical Science
基 金:江西省重点研发计划项目(20171BBG70054)~~
摘 要:目的:建立在体大鼠肺缺血/再灌注(ischemia/reperfusion,IR)损伤模型,探讨呼吸性酸中毒酸化预处理对基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)表达的影响及其机制。方法:36只雄性Sprague Dawley大鼠分为对照组(S组)、IR组和实验组(RA组),每组12只。S组开胸游离左肺门,未行阻断;IR组阻断肺门45 min后再灌注180 min;RA组游离左肺门后,调节呼吸参数,使呼气末二氧化碳压力(pressure of end tidal carbon dioxide,PETCO2)达到56~65 mmHg(1 mmHg=0.133 kPa)并维持5 min,然后同IR组处理。计算肺湿干重比值(wet/dry,W/D)和肺通透指数(lung ermeability index,LPI),进行肺组织病理学观察,并检测MMP-9蛋白的表达。结果:与S组相比,IR组和RA组在IR后W/D和LPI均上升(均P<0.05),RA组W/D和LPI升高的程度低于IR组(P<0.05);RA组肺LPI和病理学评分较IR组显著降低(均P<0.01)。IR后,与S组相比,IR组和RA组肺组织MMP-9表达明显增加(均P<0.01),但RA组肺组织MMP-9蛋白表达明显低于IR组(P<0.01)。结论:肺IR损伤后MMP-9蛋白表达增强,血管通透性增加,炎性渗出增加,呼吸性酸中毒酸化预处理能抑制MMP-9蛋白表达,减少大鼠肺IR损伤后的炎性渗出,对肺IR损伤具有保护作用。Objective: To establish rat model of lung ischemia/reperfusion(IR) in vivo, and to explore the effects of acidification pretreatment for respiratory acidosis on the expression of matrix metalloproteinase-9(MMP-9) and the possible mechanisms. Methods: A total of 36 male Sprague-Dawley rats were divided into a sham group(S group), a IR group, and an experiment group(RA group)(n=12 in each group). The rat left lung hilum in the S group was dissociated, followed by perfusion without ischemia. After the left lung hilum in the IR group was blocked for 45 min, the rats were followed by reperfusion for 180 min. After left lung hilum in the RA group was dissociated, the respiratory parameters were adjusted so that pressure of end tidal carbon dioxide(PETCO2) reached 56–65 mmHg(1 mmHg=0.133 kPa) for 5 min, then the rats was subjected to IR. Lung tissue wet/dry(W/D) and lung permeability index(LPI) were calculated, while the lung histopathology was observed and the MMP-9 protein expression were measured. Results: Compared with the control group, the W/D and LPI in the IR group and the RA group increased after reperfusion(both P<0.05), and the levels of W/D and LPI in the group RA were lower than that in the IR group(P<0.05). LPI and pathology scores were significantly lower in the RA group than those in the IR group(both P<0.01). After IR, the expression of MMP9 in the lung tissues in the IR group and the RA group increased significantly(both P<0.01). The expression of MMP-9 protein in the RA group was significantly lower than that in the IR group(P<0.01). Conclusion: After lung IR injury, the expression of MMP-9 protein, vascular permeability and inflammatory exudation is increased. The acidification pretreatment for respiratory acidosis can inhibit the expression of MMP-9 protein and reduce inflammatory exudation after lung IR, showing a protective effect on lung IR injury.
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