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目的:探讨不同潮气量（VT）机械通气对油酸（OA）诱导急性呼吸窘迫综合征（ARDS）大鼠右心血流动力学的影响。方法:将60只雄性SD大鼠按随机数字表法分为对照组（n n＝20）、ARDS模型组（n n＝20）、小VT组（n n＝10）和大VT组（n n＝10）。经大鼠颈总静脉注入OA 0.15 mL/kg制备ARDS模型；对照组给予等量生理盐水。ARDS模型组制模后2 h取10只大鼠测定氧合指数（PaOn 2/FiOn 2）；取肺组织测定湿/干重比值（W/D），光镜下观察肺组织病理学改变并进行肺损伤评分，以确定模型制备是否成功。小VT组和大VT组于制模后2 h分别给予大鼠VT为6 mL/kg或20 mL/kg的机械通气4 h；对照组和ARDS模型组保持自主呼吸。机械通气4 h后，测定大鼠心率（HR）、右心室收缩压（RVSP）、右室内压上升最大速率（dp/dt max）和血压（BP），同时取动脉血进行血气分析〔pH值、动脉血氧分压（PaOn 2）、动脉血二氧化碳分压（PaCOn 2）、PaOn 2/FiOn 2〕。n 结果:制模后1 h，ARDS模型组大鼠即出现呼吸窘迫症状。制模后2 h，大体观察可见肺脏外观有明显点片状出血；对照组无上述改变。ARDS模型组大鼠PaOn 2/FiOn 2较对照组显著降低〔mmHg（1 mmHg＝0.133 kPa）：294.3±5.9比459.0±4.4，n P<0.01〕，肺W/D比值和肺损伤评分均较对照组明显升高〔肺W/D比值：8.24±0.25比4.48±0.13，肺损伤评分（分）：0.60±0.03比0.12±0.02，均n P<0.01〕，提示ARDS模型制备成功。ARDS模型组大鼠动脉血气分析及血流动力学指标均较对照组明显恶化。机械通气4 h后，小VT组动脉血气分析指标均明显优于ARDS模型组和大VT组〔pH值：7.36±0.02比7.24±0.02、7.13±0.01，PaOn 2（mmHg）：92.4±2.1比61.8±2.3、76.6±2.2，PaCOn 2 （mmHg）：49.6±1.7比61.8±1.8、33.6±1.3，PaOn 2/FiOn 2（mmHg）：440.0±10.2比274.3±21.4、364.7±10.5，均n P<0.05〕；小VT组HR、BP和dp/dt max明显高于ARDS模型组和大VT组〔HR（次/min）：346.9±5.4比302.3±10.1、265.5±12.2，BP（mmHg）：125.4±2.2比110.0±2.5、89.2±2.8，dp/dt max（mmHg/s）：1 393.3±30.3比1 236.4±20.5、896.1±19.5，均n P<0.05〕，而RVSP则明显低于ARDS模型组和大VT组（mmHg：31.3±0.4比34.0±1.0、38.8±0.9，n P<0.05）。n 结论:小VT机械通气可改善ARDS大鼠右心室的血流动力学参数，保护右心功能。“,”Objective: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).Methods:Sixty adult male Sprague-Dawley (SD) rats were divided into control group (n n = 20), ARDS model group (n n = 20), low VT (LVT) group (n n = 10) and high VT (HVT) group (n 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 (PaOn 2/FiOn 2) 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 (PaOn 2), arterial partial pressure of carbon dioxide (PaCOn 2) and PaOn 2/FiOn 2.n Results: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 PaOn 2/FiOn 2 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, n 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 n 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 n 2 (mmHg): 92.4±2.1 vs. 61.8±2.3, 76.6±2.2; PaCOn 2 (mmHg): 49.6±1.7 vs. 61.8±1.8, 33.6±1.3; PaOn 2/FiOn 2 (mmHg): 440.0±10.2 vs. 274.3±21.4, 364.7±10.5; all n 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 n 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 n P < 0.05).n Conclusion: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.