Liu Jun, Zhang Hui, Shi Ying, Wang Tingting, Zuo Xiangrong
Department of Critical Care Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu, China. Corresponding author: Zuo Xiangrong, Email:
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2021 Jan;33(1):49-52. doi: 10.3760/cma.j.cn121430-20200710-00513.
To explore the effect of different tidal volumes (VT) on the hemodynamics of right heart in acute respiratory distress syndrome (ARDS) rats induced by oleic acid (OA).
Sixty adult male Sprague-Dawley (SD) rats were divided into control group (n = 20), ARDS model group (n = 20), low VT (LVT) group (n = 10) and high VT (HVT) group (n = 10) by random number table. ARDS model was reproduced by injecting OA 0.15 mL/kg through a jugular vein. The control group was given the same amount of normal saline. The success of modeling was judged by the oxygenation index (PaO/FiO) 2 hours after modeling, at the same time, the lung tissues were collected, the wet/dry weight (W/D) ratio was determined, and the lung histopathological changes were measured by lung injury score. The rats in the LVT group and HVT group were given mechanical ventilation with VT of 6 mL/kg or 20 mL/kg for 4 hours, respectively at 2 hours after modeling. The rats in the control group and the ARDS model group maintained spontaneous breathing. After mechanical ventilation for 4 hours, the heart rate (HR), right ventricular systolic pressure (RVSP), the maximum rate of rising of right ventricular pressure (dp/dt max), and the blood pressure (BP) were measured. Meanwhile, arterial blood samples were collected for blood gas analysis, including pH value, arterial partial pressure of oxygen (PaO), arterial partial pressure of carbon dioxide (PaCO) and PaO/FiO.
The rats in the ARDS model group showed symptoms of respiratory distress 1 hour after modeling, and the lung tissue samples showed obvious patchy bleeding 2 hours after modeling, while the control group showed no such changes. The PaO/FiO in the ARDS model group was significantly lower than that in the control group [mmHg (1 mmHg = 0.133 kPa): 294.3±5.9 vs. 459.0±4.4, P < 0.01], and the lung W/D ratio and lung injury score were significantly higher (lung W/D ratio: 8.24±0.25 vs. 4.48±0.13, lung injury score: 0.60±0.03 vs. 0.12±0.02, both P < 0.01). It indicated that ARDS model was successfully reproduced. The arterial blood gas analysis and hemodynamic parameters of the ARDS model group were significantly worse than those of the control group. After 4-hour mechanical ventilation, the blood gas parameters of the LVT group were better than those of the ARDS model group and the HVT group [pH value: 7.36±0.02 vs. 7.24±0.02, 7.13±0.01; PaO (mmHg): 92.4±2.1 vs. 61.8±2.3, 76.6±2.2; PaCO (mmHg): 49.6±1.7 vs. 61.8±1.8, 33.6±1.3; PaO/FiO (mmHg): 440.0±10.2 vs. 274.3±21.4, 364.7±10.5; all P < 0.05]. HR, BP and dp/dt max in the LVT group were significantly higher than those in the ARDS model group and the HVT group [HR (bpm): 346.9±5.4 vs. 302.3±10.1, 265.5±12.2; BP (mmHg): 125.4±2.2 vs. 110.0±2.5, 89.2±2.8; dp/dt max (mmHg/s): 1 393.3±30.3 vs. 1 236.4±20.5, 896.1±19.5; all P < 0.05], and RVSP was significantly lower than that in the ARDS model group and the HVT group (mmHg: 31.3±0.4 vs. 34.0±1.0, 38.8±0.9, both P < 0.05).
Mechanical ventilation with low VT can improve the hemodynamic parameters of the right ventricle and protect the function of the right heart in ARDS rats.
探讨不同潮气量（VT）对油酸（OA）诱导的急性呼吸窘迫综合征（ARDS）大鼠右心血流动力学的影响。
将60只成年雄性Sprague-Dawley（SD）大鼠通过随机数字表法分为对照组（n = 20）、ARDS模型组（n = 20）、低潮气量（LVT）组（n = 10）和高潮气量（HVT）组（n = 10）。经颈静脉注射0.15 mL/kg OA复制ARDS模型，对照组给予等量生理盐水。建模后2小时通过氧合指数（PaO/FiO）判断建模是否成功，同时采集肺组织，测定湿/干重（W/D）比值，通过肺损伤评分评估肺组织病理学变化。建模后2小时，LVT组和HVT组大鼠分别给予6 mL/kg或20 mL/kg VT机械通气4小时，对照组和ARDS模型组大鼠维持自主呼吸。机械通气4小时后，测量心率（HR）、右心室收缩压（RVSP）、右心室压力最大上升速率（dp/dt max）和血压（BP）。同时采集动脉血样本进行血气分析，包括pH值、动脉血氧分压（PaO）、动脉血二氧化碳分压（PaCO）和PaO/FiO。
ARDS模型组大鼠建模后1小时出现呼吸窘迫症状，建模后2小时肺组织样本出现明显片状出血，而对照组未见此类变化。ARDS模型组的PaO/FiO显著低于对照组[mmHg（1 mmHg = 0.133 kPa）：294.3±5.9 vs. 459.0±4.4，P < 0.01]，肺W/D比值和肺损伤评分显著高于对照组（肺W/D比值：8.24±0.25 vs. 4.48±0.13，肺损伤评分：0.60±0.03 vs. 0.12±0.02，均P < 0.01），表明ARDS模型复制成功。ARDS模型组的动脉血气分析和血流动力学参数显著差于对照组。机械通气4小时后，LVT组的血气参数优于ARDS模型组和HVT组[pH值：7.36±0.02 vs. 7.24±0.02，7.13±0.01；PaO（mmHg）：92.4±2.1 vs. 61.8±2.3，76.6±2.2；PaCO（mmHg）：49.6±1.7 vs. 61.8±1.8，33.6±1.3；PaO/FiO（mmHg）：440.0±10.2 vs. 274.3±21.4，364.7±10.5；均P < 0.05]。LVT组的HR、BP和dp/dt max显著高于ARDS模型组和HVT组[HR（bpm）：346.9±5.4 vs. 302.3±10.1，265.5±12.2；BP（mmHg）：125.4±2.2 vs. 110.0±2.5，89.2±2.8；dp/dt max（mmHg/s）：1 393.3±30.3 vs. 1 236.4±20.5，896.1±19.5；均P < 0.05]，RVSP显著低于ARDS模型组和HVT组（mmHg：31.3±0.4 vs. 34.0±1.0，38.8±0.9，均P < 0.05）。
低潮气量机械通气可改善ARDS大鼠右心室血流动力学参数，保护右心功能。
