通过制作改良腹腔高压（兔）液体动物模型，探索腹腔间隔室综合征（ACS）继发心脏和肺脏病理变化的特点。

将25只新西兰兔随机分为3组，对照组5只，实验1组10只，实验2组10只，分别制作改良腹腔高压液体动物模型。对照组加压水囊不注液，维持压力为0 mmHg（1 mmHg=0.133kPa）,观察48 h；实验组记录腹腔压力和腹腔增容量测定值，绘制腹腔压力-腹腔增容量曲线，腹腔压力调节在25 mmHg，实验1组观察24 h，实验2组观察48 h。在到达观察时限后处死实验兔，完整取出心脏和肺脏，用10%甲醛溶液固定24 h后常规石蜡包埋、切片、HE染色，在生物光学显微镜下观察病理改变。对实验组兔腹腔压力与腹腔增容量的关系进行简单线性回归分析。

对照组5只实验兔均存活，实验1组10只兔死亡1只，实验2组10只兔死亡2只。实验组兔腹腔压力与腹腔增容量存在正相关关系（r²=0.8023，P=0.0064），腹腔压力-腹腔增容量曲线函数方程：Y=0.1642X-132.0000。各实验组兔心脏病理变化：对照组：心肌纤维呈短圆柱状，有分支，相互连接成网；可见闰盘，呈着色较深的横行粗线。实验1组：心肌结构尚正常，心肌纤维变细，心肌间小血管扩张充血，心肌肌束萎缩，萎缩的肌细胞核聚集。实验2组：心肌间小动脉扩张充血，管腔内可见均匀一致的粉染物,心肌间静脉扩张出血，血管壁玻璃样变。各实验组兔肺脏病理变化：对照组：正常肺脏内可见终末细支气管和大量肺泡，间质内小血管扩张。实验1组：肺泡上皮增生，肺泡间隔大小不一，小灶肺泡腔融合；肺泡组织间出血，可见暗褐色物质沉积。血管内血栓，可见机化再通。实验2组：肺泡明显扩张，部分肺泡腔融合，肺泡间隔不一；终末细支气管腔内可见大量红细胞及纤维素样渗出物，其中有暗褐色物质沉积。

ACS可造成严重的心脏和肺脏损伤，随着时间延长损伤加重，这可能是ACS直接致死因素。

To explore the characteristics of pathological changes in the heart and lungs secondary to abdominal compartment syndrome (ACS) by developing an improved rabbit model of abdominal hypertension.

Twenty-five New Zealand rabbits were divided into three groups: control group (n=5), experiment group 1 (n=10), and experiment group 2 (n=10). An improved animal model of abdominal hypertension was establishing by injecting liquid. No liquid was injected for rabbits in the control group, the pressure was maintained at 0 mmHg (1 mmHg=0.133kPa), and the animals were observed for 48 hours. In the experimental groups, the abdominal pressure and the abdominal volume increase were measured to plot the pressure-volume increase curve. The abdominal pressure was then adjusted to 25 mmHg, the experiment group 1 was observed for 24 hours, and the experiment group 2 was observed for 48 hours. After the observation time limit was reached, the experimental rabbits were killed, and the heart and lungs were completely removed, fixed with 10% formalin for 24 hours, paraffin-embedded, sliced, HE-stained, and observed under an optical microscope. The relationship between abdominal pressure and volume increase in experimental rabbits was analyzed by simple linear regression.

The five rabbits in the control group all survived, 1 rabbit in the experimental group 1 and 2 in the experimental group 2 died. There was a positive correlation between abdominal pressure and volume increase (r²=0.8023, P=0.0064). The function equation was: Y=0.1642X-132.0000. Regarding pathological changes in the heart, the rabbits in the control group showed short, cylindrical myocardial fibers, branched and interconnected into nets; in the experimental group 1, the myocardial structure was normal, the myocardial fibers became thinner, the small vessels became dilated and congested, the myocardial bundles became atrophied, and the nuclei of atrophied myocardial cells gathered; in the experimental group 2, there were dilated and congested small arteries of the myocardium, uniform granules in the lumen, dilated veins of the interventricular veins, and vitreous degeneration of the blood vessels. With regard to pathological changes in the lungs, the rabbits in the control group showed terminal bronchioles and a large number of alveoli in the lungs, and dilated small vessels in the interstitium; in the experimental group 1, alveolar epithelial hyperplasia, inhomogeneous alveolar septum size, small alveolar cavity fusion, alveolar tissue bleeding, and dark brown matter deposition as well as organization and recanalization of intravascular thrombus were visible; in the experimental group 2, the alveoli were dilated obviously, some alveolar cavities were fused, the alveolar septum was inhomogeneous, and a large number of red cells and cellulosic exudates were found in the terminal fine bronchioles, in which dark brown matter was deposited.

ACS can cause severe heart and lung injury, and the injury aggravates as time goes on. This may be a direct lethal factor.