Experimental study on the pathological changes in lung of abdominal compartment syndrome model rabbits

Abstract

To investigate the secondary pathological changes in lung of abdominal compartment syndrome (ACS). Twenty-five healthy adult clean New Zealand rabbits were randomly divided into control group (n = 5) and experimental group (n = 20) according to the random number table method. The experimental group was subdivided into two subgroups according to the observation time: 24 hours and 48 hours, with 10 rabbits in each subgroup. A high pressure liquid animal model of abdominal cavity was reproduced by water bag superposition pressurization. In the control group, the pressurized water bag did not inject liquid, and intra-abdominal pressure (IAP) was maintained at 0; while in the experimental group, pressurized water infusion was performed, and IAP was maintained at 25 mmHg (1 mmHg = 0.133 kPa). The rabbits in the control group were sacrificed at 48 hours, those in the experimental group were sacrificed at 24 hours and 48 hours respectively, and the lungs were harvested completely. The pathological changes were observed under light microscope after hematoxylin-eosin (HE) staining. In the control group, the activity of the rabbits was decreased, the food intake was decreased, and all the 5 animals survived; in the experimental group, the activity was decreased significantly, little food intake or not, the urine output was decreased significantly, and 1 rabbit died at 22, 27 and 37 hours respectively, and 17 survived. Light microscopy showed that there were terminal bronchioles and a large number of alveoli in the lung tissue of the control group, and small vessels dilated in the interstitium. In the experimental group, alveolar epithelial hyperplasia, alveolar septum of different sizes, alveolar fusion, alveolar septal bleeding, interstitial heart failure cells with phagocytosis of hemosiderin, bronchiolectasis, a large number of inflammatory cell infiltration near the bronchi, thrombosis in the blood vessels were found at 24 hours. A large number of erythrocyte and cellulose-like exudates were seen in the lumen of terminal bronchioles, alveolar dilatation and fusion were aggravated, and old hemorrhage in the lumen of the alveoli was observed, hemosiderosis containing hemosiderin was observed at 48 hours. ACS could cause severe lung injury and aggravate as time goes on.