Effect of mechanical ventilation on pressure-volume relationship of abdominal cavity in a modified abdominal hypertension liquid animal model

Abstract

Objective To explore the effect of mechanical ventilation on the pressure-volume relationship of abdominal cavity via making an improved abdominal hypertension liquid animal model by means of water bag superposition pressurization. Methods 12 experimental pigs were randomly divided into group A (mechanical ventilation group) and group B (non mechanical ventilation group), 6 pigs in each group. Both groups were anesthetized under general anesthesia. In group A, ventilator was used to assist breathing after tracheal intubation. The breathing mode was volume controlled ventilation (VCV), tidal volume (VT) 10 ml/kg, breathing rate 16 times/min, inhaled oxygen concentration (FiO2) 0.40, positive end expiratory pressure (PEEP) 5 cm H2O(1 cmH2O=0.098 kPa). The abdominal hypertensive fluid models of group A and group B were made according to the operation procedure of the abdominal hypertensive fluid model made by the water sac method, the abdominal hypertensive fluid models of group A and group B were injected with normal saline through the drainage pipe of the drainage bag, the abdominal pressure was measured once every 10 ml, the total fluid volume was recorded, the abdominal pressure was recorded synchronously, and the abdominal pressure increase curve was drawn. The volume of fluid injection was recorded when the abdominal pressure was 0, 10, 20, 30, 40, 50 cm H2O (0 refers to the zero point of abdominal pressure rise). The intraabdominal pressure was maintained at 35 cmH2O (25.74 mmHg). After 4 hours of observation, the experimental animals were killed, the hearts and lungs were harvested and fixed with 10% formaldehyde solution for 24 hours. The samples were embedded in paraffin and stained with HE. Results All 12 pigs were successfully moulded without barometric injury or death. In group A, the abdominal pressure-volume increase curve was an irregular S hyperfunction curve. The turning point of abdominal pressure 22 cm H2O, there was a positive correlation between the abdominal pressure and volume increase when the abdominal pressure was less than 22 cm H2O (r2=0.78, P<0.05), and the abdominal pressure was positively correlated with the volume increase when the abdominal pressure was more than 22 cm H2O (r2=0.96, P<0.01). In group B showed that there was a positive correlation between abdominal pressure and volume increase (r2=0.87, P<0.01). While the intraperitoneal pressures of group A were 0, 10, 20, 30, 40, 50 cm H2O, the amounts of fluid of group A [(2 018.22±108.66)ml, (2 032.60±114.42)ml, (2 038.54±112.60)ml, (2 080.88±118.44)ml, (2 162.38±118.86)ml, (2 310.78±124.20)ml] were significantly lower than those of group B [(2 890.40±164.50)ml, (3 000.58±176.22)ml, (3 060.24±178.24)ml, (3 098.50±183.40)ml, (3 120.00±184.20)ml, (3 145.80±188.60)ml], there were statistical significances (t=4.42, 4.61, 4.85, 4.66, 4.37, 5.35, all P<0.01). Cardiological examination: in group A, myocardial fibers with hyaline degeneration, reduced transverse striation model, and partial atrophy of myocardial fibers could be seen. In group B, partial atrophy and hypertrophy of cardiac myocardial fibers, hyaline degeneration of myocardial fibers, dilatation and congestion of myocardial arteries could be seen. Lung pathology examination: in group A, alveolar lumen of different sizes can be seen in the lungs. There was part alveolar fusion, alveolar cavity dilatation, bleeding, chronic inflammatory cell infiltration and inflammatory exudation between lung tissues, smooth muscle proliferation around bronchioles. In group B, the pulmonary alveoli fused to form larger alveolar sacs, alveolar endothelial cells moderately proliferated, heart failure cells could be seen, interstitial lymphatic vessels dilated, lymphatic vessels were filled with lymph, bronchial artery dilated and congested, and a large number of red blood cells accumulated in the lumen. Conclusion Abdominal hypertension can cause significant cytological damage to the heart and lungs. Mechanical ventilation can reduce the compensatory space of abdominal compartment syndrome (ACS), change the relationship between abdominal pressure and volume, and protect the heart and lung to a certain extent. Key words: Mechanical ventilation; Intraabdominal hypertension; Animal model; Water bag; Pressure-volume curve