To explore the changes of cardiac function and its mechanism in the animal model of abdominal compartment syndrome (ACS) under mechanical ventilation.

Ten healthy adult pigs was randomly divided into experimental group (N=6) and control group (N=4) according to the random number method. In the experimental group; the abdominal hypertensive liquid animal model was reproduced by water sac superimposed pressure under mechanical ventilation; in the control group, the abdomen was closed immediately after the empty pressurized water sac was placed along the abdominal incision after anesthesia. Mechanical ventilation was set in volume controlled ventilation (VCV) mode with tidal volume (VT) 10 mL/kg, respiratory frequency 16 times/min, inhaled oxygen concentration (Fi02) 40%, and positive end-expiratory pressure (PEEP) 5 cm H₂O (1 cmH₂O= 0.098 kPa). 0.9% sodium chloride was injected into the pressurized water sac through a pressurized tube (once every 50 mL pressure measurement) until the intraperitoneal pressure reached 30 mmHg (1 mmHg = 0.133 kPa). The pressure-volume curve was recorded and drawn. The intraperitoneal pressure was maintained at 25 mmHg after partial injection. The intraperitoneal pressure was continuously observed for 4 hours before and after the establishment of the model, respectively. After maintenance, 5 ml of venous blood was drawn from ear vein every hour, and myocardial enzymogram was performed. After modeling and maintaining abdominal pressure for 4 hours, the animals were killed by intravenous injection of propofol. The hearts were cut intact. The hearts were fixed in 10% formaldehyde solution for 24 hours and embedded in paraffin. Coronal sections were made continuously (4 microns thick). The hearts were stained with hematoxylin-eosin (HE) and the pathological changes of myocardium were observed under bio-optical microscope (x 200).

The intraabdominal pressure of abdominal hypertension liquid (pig) animal model was positively correlated with abdominal volume increasing, and the abdominal pressure abdominal volume curve was a linear function. The function equation was Y=0.1074X-206.045 (r²=0.8396, P<0.05). Compared with before modeling, lactate dehydrogenase (LDH), creatine kinase isoenzyme (CK-MB) and α-hydroxybutyrate dehydrogenase (alpha-HBDH) increased 1 h after modeling (all P<0.05), but there was no significant difference in each index between 2 and 4 h after modeling. Under mechanical ventilation, ACS resulted in eosinophilic degeneration, atrophy, hypertrophy, disappearance of transverse lines, vitreous degeneration and nuclear aggregation in myocardial fibers.

Mechanical ventilation changes the shape of pressure-volume curve of ACS. The development of ACS under mechanical ventilation is accompanied by myocardial cell injury and myocardial enzymogram changes.