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目的:通过对比分析采用多水囊叠加加压法制备腹腔高压的“定容”动物模型与气体灌注法制备的“定压”动物模型，筛选更符合临床腹腔间隔室综合征（ACS）病变规律的动物模型制备方法。方法:选择10只健康家猪，按随机数字表法分为两组，每组5只。分别采用水囊叠加加压法制备腹腔高压“定容模型”（定容模型组）和采用人工气腹法制备腹腔高压“定压模型”（定压模型组），两组腹腔压力均为25 mmHg（1 mmHg＝0.133 kPa），制模后观察4 h，每小时测压1次，测压结果取均值，绘制腹腔压力-时间变化曲线。制模后4 h处死动物取心脏和肺脏，用苏木素-伊红（HE）染色，镜下观察组织病理学改变。结果:两组实验猪均成功制模。定容模型组术后0、1、2、3、4 h腹腔压力值逐渐升高（mmHg：分别为25.0±0、27.1±0.2、29.4±0.1、30.9±0.2、33.1±0.1），腹腔压力与时间呈正相关关系（函数方程：n Y1＝25.102 0+1.996 0n X1，n R2＝0.996 2，n P＝0.000 1）。定压模型组术后所有时间点腹腔压力值均维持在25 mmHg，腹腔压力与时间无线性相关关系（函数方程：n Y2＝25）。HE染色显示，定容模型组心肌纤维伴玻璃样变性，横纹明显减少，部分心肌纤维萎缩，可见细胞核聚集；肺组织可见出血，有慢性炎性细胞浸润及炎性渗出。定压模型组心肌纤维部分萎缩，部分肥大，局灶可见玻璃样变性，局灶横纹消失，心肌间动脉扩张充血；肺泡上皮部分区域轻度增生，可见心衰细胞，支气管动脉可见扩张充血，管腔内见大量红细胞及均匀一致的淡染物质。n 结论:多水囊叠加加压法制备腹腔高压“定容”动物模型，在制模后腹腔压力随疾病的发展持续动态升高，符合临床ACS病变规律，比“定压”动物模型更适合科研时制备腹腔高压动物模型。“,”Objective:To select the animal model more consistent with the pathophysiology of abdominal compartment syndrome (ACS) through the comparative study of the methods of multiple water sacs superimposed compression and gas perfusion.Methods:Ten experimental pigs were randomly divided into two groups (n n = 5): the “constant volume model” (constant volume model group) and the “constant pressure model” (constant pressure model group) of intra-abdominal hypertension. The models were prepared by the method of water sac superposition and pressurization, and artificial pneumoperitoneum respectively. The abdominal pressures of both groups were 25 mmHg (1 mmHg = 0.133 kPa) and observed for 4 hours. The pressure was measured once an hour for 4 hours and the pressure-time curves of the two groups were drawn respectively. The experimental animals were sacrificed 4 hours after modeling. The heart and lung were harvested, and the histopathological changes were observed by hematoxylin-eosin (HE) staining.n Results:Two groups of experimental pigs were successfully modeled. The abdominal pressure gradually increased at 0, 1, 2, 3, 4 hours after operation in the constant volume model group (mmHg: 25.0±0, 27.1±0.2, 29.4±0.1, 30.9±0.2, 33.1±0.1), and there was a positive correlation between the abdominal pressure and time (functional equation: n Y1 = 25.102 0+1.996 0n X1; n R2 = 0.996 2, n P = 0.000 1). The abdominal pressure value in the constant pressure model group at 0, 1, 2, 3, 4 hours were maintained 25 mmHg, and there was no linear correlation between the abdominal pressure and time (functional equation: n Y2 = 25). HE staining showed that in the constant volume model group, the myocardial fibers were accompanied with hyaline degeneration, significantly reduced transverse lines, part of myocardial fiber atrophy, and visible nuclear aggregation; hemorrhage, chronic inflammatory cell infiltration and inflammatory exudation were found in the lung tissues. In the constant pressure model group, partial atrophy of myocardial fiber, partial hypertrophy, focal hyaline degeneration, disappearance of local striae, hyaline degeneration of myocardial fiber, dilation and congestion of intermyocardial artery were observed. Slight hyperplasia of alveolar epithelium in some areas, heart failure cells, dilation and congestion of bronchi and trachea artery, a large number of red blood cells and uniform light staining substances in lumen were found.n Conclusion:After the model was made by the method of multiple water sacs, the pressure of the abdominal cavity continued to increase with the development of the disease, which was in line with the clinical pathological changes of ACS, and was more suitable for making the animal model of the intra-abdominal hypertension.