逐渐性增加潮气量可减轻大鼠实验性肺损伤
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Gradually Increasing Tidal Volume May Mitigate Experimental Lung Injury in Rats
背景与目的
对于轻度急性呼吸窘迫综合征，高潮气量（VT）可产生一定程度的肺损伤；本研究假设如果VT缓慢增加，可减少机械异质性并使肺泡上皮细胞和内皮细胞以及细胞外基质产生适应性，则肺损伤可以减轻。故本研究本研究旨在探讨逐渐增加潮气量的不同方式对大鼠实验性肺损伤的影响 。
方 法
64只Wistar大鼠气管内注射大肠杆菌脂多糖，制备急性呼吸窘迫综合征模型。 24小时后，随机分为四组，并进行机械通气：对照组:VT=6ml/kg，持续2h；无适应时间组：第1小时VT=6ml/kg，第2小时VT突然增加至22ml/kg；短适应时间组：前30分钟内VT为6ml/kg，随后30分钟内VT逐渐增加至22ml/kg，然后在第2小时内VT恒定为22ml/kg； 长适应时间组：在第1小时，VT从6ml/kg增加到22ml/kg，在第2小时，VT恒定为22ml/kg。所有动物均接受3cmH2O的呼气末正压通气，分子生物学技术检测相关分子指标。
结 果
2 h时，长适应时间组弥漫性肺泡损伤评分和异质性指数较对照组及短适应时间组高；长适应时间组白细胞介素-6的表达较对照组及短适应时间组表达水平多（长适应时间组：76.7[20.8–95.4]；短适应时间组12.4[9.1–17.8]：；对照组：65.5[18.1–129.4;p=0.02.）;双调蛋白、基质金属蛋白酶-9、细胞分泌蛋白-16和多配体蛋白聚糖表达在各组间与前述一致。
结 论
在实验性轻度急性呼吸窘迫综合征大鼠模型，与无适应时间组相比，短适应时间组的肺损伤可通过肺泡上皮细胞和细胞外基质的方式得以减轻；延长适应期可增加累积能量，但不能防止肺损伤。
原始文献摘要
Nathane S. Felix, Cynthia S. Samary,Fernanda F.Cruz,etal;Gradually Increasing Tidal Volume May Mitigate Experimental Lung Injury in Rats;Anesthesiology 2019; 130:767–77.
Background: This study hypothesized that, in experimental mild acute respiratory distress syndrome, lung damage caused by high tidal volume (VT) could be attenuated if VT increased slowly enough to progressively reduce mechanical heterogeneity and to allow the epithelial and endothelial cells, as well as the extracellular matrix of the lung to adapt. For this purpose, different strategies of approaching maximal VT were tested.
Methods: Sixty-four Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 h, animals were randomly assigned to receive mechanical ventilation with VT = 6 ml/kg for 2 h (control); VT = 6 ml/kg during hour 1 followed by an abrupt increase to VT = 22 ml/kg during hour 2 (no adaptation time); VT = 6 ml/kg during the first 30 min followed by a gradual VT increase up to 22 ml/kg for 30 min, then constant VT = 22 ml/kg during hour 2 (shorter adaptation time); and a more gradual VT increase, from 6 to 22 ml/kg during hour 1 followed by VT = 22 ml/kg during hour 2 (longer adaptation time). All animals were ventilated with positive end-expiratory pressure of 3 cm H2O. Nonventilated animals were used for molecular biology analysis.
Results: At 2 h, diffuse alveolar damage score and heterogeneity index were greater in the longer adaptation time group than in the control and shorter adaptation time animals. Gene expression of interleukin-6 favored the shorter (median [interquartile range], 12.4 [9.1–17.8]) adaptation time compared with longer (76.7 [20.8 to 95.4]; P = 0.02) and no adaptation (65.5 [18.1 to 129.4]) time (P = 0.02) strategies. Amphiregulin, metalloproteinase-9, club cell secretory protein-16, and syndecan showed similar behavior.
Conclusions: In experimental mild acute respiratory distress syndrome, lung damage in the shorter adaptation time group compared with the no adaptation time group was attenuated in a time-dependent fashion by preemptive adaptation of the alveolar epithelial cells and extracellular matrix. Extending the adaptation period increased cumulative power and did not prevent lung
damage, because it may have exposed animals to injurious strain earlier and for a longer time, thereby negating any adaptive benefit.
麻醉学文献进展分享
贵州医科大学高鸿教授课题组
翻译：王贵龙 编辑：何幼芹 审校：王贵龙