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.