摘要
目的动态观察部分液体通气（PLV）对内毒素诱导急性肺损伤（ALI）幼猪促炎／抗炎因子的影响。方法选择12头上海小白猪，按随机数字表法分为单纯机械通气（MV）组和PLV组，每组6头。静脉输注内毒素60μg·kg-1·h-静脉维持2h诱导Au模型。PLV组在MV基础上气管内注入全氟萘烷（PFC）10mL／kg。两组分别于基础状态下和ALI模型制备成功后0、1、2、4h时监测血流动力学、呼吸力学、动脉血气分析等参数，并采用酶联免疫吸附试验（ELISA）动态检测血清白细胞介素（IL-1B、IL-6、IL-8、IL-10）和肿瘤坏死因子-α．（TNF-OL）的水平；光镜下观察肺组织病理学改变，并进行病理学评分。结果PLV组给药后通气和氧合功能逐渐改善，气道阻力下降，在成模4h时各指标与MV组比较差异均有统计学意义[心率（HR，次／rain）：144±6比179±9，呼吸频率（RR，次／min）：58±4比77±6，平均动脉压（MAP，mmHg，1mmHg=O．133kPa）：99±7比75±29，肺顺应性（Cdyn，mL·cmH202·kg-1：1．9±0．3比1．2±0．4，潮气量（VT,mL／kg）：7．8±0．4比5．8±0．9，平均气道阻力（Raw，emH20·L-1·S-1）：20．5±6．6比35．2±4．0，平均气道压（Paw，emil20，1emil20=0．098kPa）：1．0±0．5比3．0±0．9，通气效率指标（VEI）：0．18±0．02比0．08±0．02，pH值：7．386±0．143比7．148±0．165，动脉血氧分压（PaO2，mmHg）：121．8±12．5比73．6±10．9，动脉血二氧化碳分压（PaCO：，mmHg）：39．6±20．3比66．8±23．5，氧合指数（Pa02／FiO：，mmHg）：311±35比184±27，P〈O．05或P〈O．01]。两组成模时血清TNF-α．、IL-1β、IL-6、IL-8、IL-10均较基础状态时明显升高，且随时间延长逐渐上升，成模后各时间点PLV组促炎因子明显低于MV组，以4h时最为明显[TNF-α（ng／L）：98．4±21．1比178．0±55．0，IL-β（ng／L）：142．0±38．0比226．0±55．0，IL-6（ng／L）：763．0±282．0比1303．0±260．0，IL-8（ng／L）：1183．0±403．0比1876．0±232．0，P〈O．05或P〈O．01]，而两组间抗炎因子IL-10差异无统计学意义（ng／L：292．0±40．0比208．0±82．0，P〉O．05）；PLV组TNF-cdIL-10比值于成模2h即显著低于MV组（0．58±0．13比1．13±0．54，P〈O．05），而IL-6／IL-10比值在成模4h显著低于MV组（2．72±1．27比7．17±3．08，P〈O．01）。光镜下观察PLV组肺内炎性细胞浸润、肺充血及问质水肿均较MV组明显改善。PLV组肺损伤评分明显低于MV组（非重力依赖区：9．8±0．8比11．8±1．0，t=3．956，P=O．003；重力依赖区：5．0±0．6比14．7±2．3，t=10．127，P=O．000）。结论PLV可显著降低Au幼猪促炎因子水平，且在维持促炎／抗炎因子平衡方面效果更明显，这可能是PLV改善肺损伤的机制之-。
Objective To evaluate the effect of partial liquid ventilation （PLV） on pro-inflammatory and anti-inflammatory factors change in lipopolysaeeharide （LPS）-indnced piglets acute lung injury （ALI）. Methods Twelve Shanghai white piglets were randomly divided into mechanical ventilation （MV） group （n = 6 ） and PLV group （n=6）. 60 μg＇kg-1 ·h-1 LPS were intravenous infused continuously for 2 hours to induce ALI model. PLV model was set on the basis of the MV by endotracheal injection of perfluorodecalin （PFC, 10 mL/kg）. The hemodynamie and respiratory parameters such as mechanics and arterial blood gas analysis were monitored at basic condition and after lung injury establishment （0, 1, 2, 4 hours）. The serum levels of interleukin （IL-113, IL-6, IL-8, IL-10） and tumor necrosis factor-α （TNF-α） were dynamically monitored by enzyme linked immuuosorbent assay （ELISA）. A lung injury score was used to quantify lung tissues change under light microscopic observations. Results Ventilation and oxygenation function were improved gradually after PFC endotracheal injection in PLV group, and there were significant difference compared with MV group at 4 hours Iheart rate （HR, beats/min） ： 144 ± 6 vs. 179 ± 9, respiratory rate （RR, beats/min） ： 58 ± 4 vs. 77 ± 6, mean arterial blood pressure （MAP, mmHg, 1 mmHg=0.133 kPa） ： 99 ± 7 vs. 75 ±29, dynamic lung compliance （Cdyn, mL·cmH20-1·kg-1 ） ： 1.9 ± 0.3 vs. 1.2 ± 0.4, tidal volume （VT, mL/kg） ： 7.8±0.4 vs. 5.8 ± 0.9, mean airway resistance （Raw, cmH20·L-1 ·s-1）： 20.5 ± 6.6 vs. 35.2 ± 4.0, mean airway pressure （Paw, cmH20, 1 cmH20=0.098 kPa）： 1.0±0.5 vs. 3.0 ±0.9, ventilation efficacy index （VEI）： 0.18 ±0.02 vs. 0.08 ± 0.02, pH value： 7.386 ± 0.143 vs. 7.148 ± 0.165, arterial partial pressure of oxygen （PaOz, mmHg）： 121.8 ± 12.5 vs. 73.6 ± 10.9, arterial partial pressure of carbon dioxide （PaCOz, mmHg）： 39.6 ± 20.3 vs. 66.8 ± 23.5, oxygenation index （PaO2/FiO2, mmHg）： 311 ± 35 vs. 184 ± 27, P〈0.05 or P〈0.011. All serum cytokines in both groups were significantly increased after LPS-induced ALI, and showed an elevated tendency. The serum pro-inflammatory factors of TNF-α , IL-Iβ, IL-6 and IL-8 in PLV group were significantly lower than those in MV group at 4 hours [TNF-α （ng/L） ： 98.4 ± 21.1 vs. 178.0 ± 55.0, IL-1[3 （ng/L） ： 142.0 ± 38.0 vs. 226.0 ± 55.0, IL-6 （ng/L） ： 763.0 ± 282.0 vs. 1 303.0 ± 260.0, IL-8 （ng/L） ： 1 183.0 ± 403.0 vs. 1 876.0 ± 232.0, P〈0.05 or P〈0.01 ]. There was no significant difference in serum anti-inflammatory factor of IL-10 between PLV and MV groups at 4 hours （ng/L： 292.0 ±-40.0 vs. 208.0 ± 82.0, P〉0.05）. The ratio of TNF-cdIL-10 in PLV group was significantly decreased compared with MV group at 2 hours （0.58 ± 0.13 vs. 1.13 ± 0.54, P〈0.05）. The ratio of IL-6/IL-10 in PLV group was significantly decreased compared with MV group at 4 hours （2.72 ± 1.27 vs. 7.17 ± 3.08, P〈0.01）. Microscopic changes in intra-alveolar and interstitial inflammation, hemorrhage and edema were better in PLV group than those in MV group. The lung injury score of PLV group was lower than MV group （ independent lung regions ： 9.8 ±0.8 vs. 11.8 ± 1.0, t=3.956, P=0.003; dependent lung regions： 5.0 ± 0.6 vs. 14.7 ± 2.3, t=10.127, P=0.000）. Conclusion PLV can significantly reduce the levels of pro-inflammatory factors and the ratio of pro-inflammatory/anti-inflammatory factor, which may contribute to the protective effects of PLV on ALI.
出处
《中华危重病急救医学》
CAS
CSCD
北大核心
2014年第2期74-79,共6页
Chinese Critical Care Medicine
基金
国家自然科学基金面上项目，上海市科委科技计划项目
关键词
肺损伤
急性
部分液体通气
机械通气
炎症反应
血流动力学
Acute lung injury
Partial liquid ventilation
Mechanical ventilation
Inflammatoryresponse
Hemodynamics
