驱动压对肺内源性急性呼吸窘迫综合征的影响

doi:10.3877/cma.j.issn.1674-6880.2018.04.005

中华危重症医学杂志(电子版) ›› 2018, Vol. 11 ›› Issue (04) : 238 -243. doi: 10.3877/cma.j.issn.1674-6880.2018.04.005

所属专题：文献；

论著

驱动压对肺内源性急性呼吸窘迫综合征的影响

杨茂宪¹, 赵文静², 王丽燕³, 孔敏⁴, 许鹏程², 徐龙生⁵, 沈辉⁵, 邓厚盛⁶, 和秋莉⁷, 施云超¹^,^†(

)

^1. 314001　浙江嘉兴，浙江省嘉兴市第一医院ICU
^2. 221002　江苏徐州，徐州医科大学附属医院ICU
^3. 314001　浙江嘉兴，嘉兴市第一医院全科病房
^4. 314001　浙江嘉兴，嘉兴市第一医院麻醉科
^5. 314001　浙江嘉兴，嘉兴市第一医院中心实验室
^6. 325000　浙江温州，温州医科大学附属第二医院麻醉科
^7. 233030　安徽蚌埠，蚌埠医学院研究生院

收稿日期:2018-01-04 出版日期:2018-08-01
通信作者: 施云超
基金资助:
嘉兴市医学重点学科（支撑学科）资助项目(04-Z-08); 嘉兴市第一医院（壹计划）资助项目(2017-YA-50)

Effect of driving pressure on pulmonary endogenous acute respiratory distress syndrome

Maoxian Yang¹, Wenjing Zhao², Liyan Wang³, Min Kong⁴, Pengcheng Xu², Longsheng Xu⁵, Hui Shen⁵, Housheng Deng⁶, Qiuli He⁷, Yunchao Shi¹^,^†()

^1. Department of Intensive Care Unit, the First Hospital of Jiaxing, Jiaxing 314001, China
^2. Department of Intensive Care Unit, the Affiliated Hospital of Xuzhou Medical University, Xuzhou 221002, China
^3. Department of General Practice, the First Hospital of Jiaxing, Jiaxing 314001, China
^4. Department of Anesthesiology, the First Hospital of Jiaxing, Jiaxing 314001, China
^5. Central Laboratory, the First Hospital of Jiaxing, Jiaxing 314001, China
^6. Department of Anesthesiology, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
^7. Graduate School of Bengbu Medical University, Bengbu 233030, China

Received:2018-01-04 Published:2018-08-01
Corresponding author: Yunchao Shi
About author:
Corresponding author: Shi Yunchao, Email: luleisyc@126.com

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引用本文：

杨茂宪, 赵文静, 王丽燕, 孔敏, 许鹏程, 徐龙生, 沈辉, 邓厚盛, 和秋莉, 施云超. 驱动压对肺内源性急性呼吸窘迫综合征的影响[J]. 中华危重症医学杂志(电子版), 2018, 11(04): 238-243.

Maoxian Yang, Wenjing Zhao, Liyan Wang, Min Kong, Pengcheng Xu, Longsheng Xu, Hui Shen, Housheng Deng, Qiuli He, Yunchao Shi. Effect of driving pressure on pulmonary endogenous acute respiratory distress syndrome[J]. Chinese Journal of Critical Care Medicine(Electronic Edition), 2018, 11(04): 238-243.

目的

探讨不同驱动压力对脂多糖诱导的肺内源性急性呼吸窘迫综合征（ARDS）的治疗作用及其机制。

方法

40只雄性Sprague-Dawley大鼠分为对照组、急性呼吸窘迫综合征模型组（ARDS组）、机械通气低驱动压组（L组）、机械通气一般驱动压组（M组）、机械通气高驱动压组（H组），每组各8只。气管内滴注脂多糖6 mg/kg复制ARDS动物模型，模型复制成功后对L组、M组及H组实施相应的机械通气策略4 h。比较5组大鼠动脉血氧分压（PaO₂）、二氧化碳分压（PaCO₂）、肺组织湿/干重比、肺泡灌洗液（BALF）中总蛋白、Ⅲ型前胶原（PCⅢ）、血清中白细胞介素6（IL-6）的表达水平以及肺组织病理形态学变化情况。

结果

5组大鼠PaO₂、PaCO₂、肺组织湿/干重比、BALF中蛋白含量、血清IL-6、PCⅢ表达水平、塌陷肺泡所占比例以及膨胀肺泡所占比例比较，差异均有统计学意义（F= 25.054、5.316、14.306、84.940、93.379、41.983、49.343、123.433，P均< 0.05）。进一步两两比较发现，L组和H组PaO₂、肺组织湿/干重比、BALF中蛋白含量、血清IL-6以及塌陷肺泡所占比例与ARDS组比较，差异均有统计学意义（P均< 0.05），H组PaCO₂表达水平和膨胀肺泡所占比例与ARDS组比较，差异均有统计学意义（P均< 0.05），L组PCIⅢ表达水平较ARDS组显著降低（P < 0.05）；H组PaO₂、血清IL-6、PCⅢ表达水平、塌陷肺泡所占比例以及膨胀肺泡所占比例与ARDS组比较，差异均有统计学意义（P均< 0.05）。

结论

在小潮气量通气下，较低的驱动压力能够改善脂多糖诱导的肺内源性ARDS大鼠的气体交换，减轻肺水肿，降低炎症反应；当驱动压过高时可能引起肺过度膨胀，甚至诱发肺损伤的发生。

关键词: 驱动压, 急性呼吸窘迫综合征, 脂多糖

Objective

To investigate the effect of different driving pressure on pulmonary endogenous acute respiratory distress syndrome (ARDS) induced by lipopolysaccharide and its mechanism.

Methods

Forty male Sprague-Dawley rats were divided into the control group, ARDS group, mechanical ventilation low driving pressure group (L group), mechanical ventilation medium driving pressure group (M group), and mechanical ventilation high driving pressure group (H group), 8 rats in each group. The ARDS model was established by intratracheal instillation of lipopolysaccharide (6 mg/kg). Then the corresponding mechanical ventilation strategies were applied to L, M and H groups for 4 h. The expressions of arterial partial pressure of oxygen (PaO₂), partial pressure of carbon dioxide (PaCO₂), wet/dry weight ratio of lung tissue (W/D), total protein in bronchoalveolar lavage fluid (BALF), type Ⅲ procollagen (PCⅢ) and interleukin 6 (IL-6) in serum, and the pathological and morphological changes of lung tissue were compared in these five groups.

Results

There were significant differences in the expressions of PaO₂, PaCO₂, wet/dry weight ratio of lung tissu, protein content in BALF, IL-6 in serum and PCⅢ, and the proportion of collapsed alveoli and inflated alveoli in these five groups (F= 25.054, 5.316, 14.306, 84.940, 93.379, 41.983, 49.343, 123.433; all P < 0.05). Further comparison showed that the expressions of PaO₂, W/D of lung tissue, protein content in BALF and IL-6 in serum, and the proportion of collapsed alveoli in L and H groups were significantly different compared with ARDS group (all P < 0.05). The expression of PaCO₂ and the proportion of inflated alveoli in H and ARDS groups were significantly different (both P < 0.05). The PCⅢ expression was significantly lower in the L group than in ARDS group (P < 0.05). The expressions of PaO₂, IL-6 in serum and PCⅢ, and the proportion of collapsed alveoli and inflated alveoli in H and ARDS groups were significantly different (all P < 0.05).

Conclusions

Under low tidal volume ventilation, lower driving pressure can improve gas exchange and reduce pulmonary edema and inflammatory response in lipopolysaccharide induced lung endogenous ARDS rats. High driving pressure may cause excessive lung expansion and lead to lung injury.

Key words: Driving pressure, Acute respiratory distress syndrome, Lipopolysaccharide

表1 不同驱动压力对5组大鼠PaO₂、PaCO₂及肺组织湿/干重的影响（±s）

组别	只数	PaO₂(mmHg)	PaCO₂(mmHg)	肺组织湿/干重
对照组	8	108 ± 17	41 ± 9	4.37 ± 0.15
ARDS组	8	55 ± 6^a	53 ± 5^a	5.32 ± 0.42^a
L组	8	79 ± 11^ab	45 ± 4^b	4.91 ± 0.35^ab
M组	8	106 ± 14^bc	43 ± 6^b	4.47 ± 0.20^bc
H组	8	93 ± 12^abc	49 ± 6^ad	4.77 ± 0.17^abd
F值	?	25.054	5.316	14.306
P值	?	< 0.001	0.002	< 0.001

表1 不同驱动压力对5组大鼠PaO₂、PaCO₂及肺组织湿/干重的影响（±s）

组别	只数	PaO₂(mmHg)	PaCO₂(mmHg)	肺组织湿/干重
对照组	8	108 ± 17	41 ± 9	4.37 ± 0.15
ARDS组	8	55 ± 6^a	53 ± 5^a	5.32 ± 0.42^a
L组	8	79 ± 11^ab	45 ± 4^b	4.91 ± 0.35^ab
M组	8	106 ± 14^bc	43 ± 6^b	4.47 ± 0.20^bc
H组	8	93 ± 12^abc	49 ± 6^ad	4.77 ± 0.17^abd
F值	?	25.054	5.316	14.306
P值	?	< 0.001	0.002	< 0.001

表2 不同驱动压力对5组大鼠BALF中总蛋白、PCⅢ以及血清IL-6表达水平的影响（±s）

组别	只数	BALF总蛋白(g/L)	PCⅢ(μg/L)	血清IL-6(ng/L)
对照组	8	0.43 ± 0.07	0.78 ± 0.22	111 ± 26
ARDS组	8	1.94 ± 0.13^a	32.85 ± 9.98	840 ± 141^a
L组	8	1.26 ± 0.28^ab	28.07 ± 5.58^a	453 ± 78^ab
M组	8	0.95 ± 0.16^abc	29.67 ± 3.62^a	278 ± 39^abc
H组	8	1.12 ± 0.12^abd	43.62 ± 9.78^abcd	366 ± 58^abcd
F值	?	84.940	41.983	93.379
P值	?	< 0.001	< 0.001	< 0.001

表2 不同驱动压力对5组大鼠BALF中总蛋白、PCⅢ以及血清IL-6表达水平的影响（±s）

组别	只数	BALF总蛋白(g/L)	PCⅢ(μg/L)	血清IL-6(ng/L)
对照组	8	0.43 ± 0.07	0.78 ± 0.22	111 ± 26
ARDS组	8	1.94 ± 0.13^a	32.85 ± 9.98	840 ± 141^a
L组	8	1.26 ± 0.28^ab	28.07 ± 5.58^a	453 ± 78^ab
M组	8	0.95 ± 0.16^abc	29.67 ± 3.62^a	278 ± 39^abc
H组	8	1.12 ± 0.12^abd	43.62 ± 9.78^abcd	366 ± 58^abcd
F值	?	84.940	41.983	93.379
P值	?	< 0.001	< 0.001	< 0.001

表3 不同驱动压力对5组大鼠肺组织病理形态学的影响（±s）

组别	只数	塌陷肺泡所占比例(%)	膨胀肺泡所占比例(%)
对照组	8	5±3	0
ARDS组	8	46 ± 11^a	0
L组	8	28 ± 6^ab	0
M组	8	21 ± 3^abc	4.8 ± 2.2^abc
H组	8	12 ± 4^abcd	12.8 ± 2.3^abcd
F值	?	49.343	123.433
P值	?	< 0.001	< 0.001

表3 不同驱动压力对5组大鼠肺组织病理形态学的影响（±s）

组别	只数	塌陷肺泡所占比例(%)	膨胀肺泡所占比例(%)
对照组	8	5±3	0
ARDS组	8	46 ± 11^a	0
L组	8	28 ± 6^ab	0
M组	8	21 ± 3^abc	4.8 ± 2.2^abc
H组	8	12 ± 4^abcd	12.8 ± 2.3^abcd
F值	?	49.343	123.433
P值	?	< 0.001	< 0.001

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