Abstract:Objective To establish a New Zealand white rabbit model of diving decompression sickness and an evaluating system for the model. Methods Twenty-five New Zealand white rabbits were subjected to a simulated dive in DWC150 animal compression chamber. After 60 min exposure to compressed air at 500 kPa, the pressure inside the chamber was decreased to normal pressure at a constant speed of 200 kPa/min. Six healthy New Zealand white rabbits were ventilated under normal pressure and set as normal control group. After decompression, the amount of gas bubbles flowing through the right ventricle was observed by ultrasonography. The amount of gas bubbles, functional status of hind limbs, respiratory function, and lung and spinal cord pathological examination results were scored, and the blood routine and coagulation function were detected. Results With this decompression program, the incidence of decompression sickness was 76% (19/25) and mortality rate was 28% (7/25). Cardiac ultrasonography showed great amount of gas bubbles in venous system of the rabbits with decompression sickness, and the gas bubble score was significantly higher than that in the normal control group (Z=-3.702, P=0.002). The rabbits with decompression sickness had abnormal hind limb motor function and respiratory function, and the Tarlov score and respiratory function score were significantly higher than those in the normal control group (Z=-2.172 and -3.702, both P<0.05). The rabbits with decompression sickness had significantly higher lung wet/dry dry mass ratio versus the normal control rabbits (t=4.52, P<0.01). H-E staining showed that the rabbits after decompression for 24 h had alveolar hemorrhage, alveolar septum thickening and vacuole-like changes of spinal cord. The white blood cell counts of the rabbits significantly increased at 6 h and 12 h after decompression (t=3.933, 2.838; P=0.003, 0.019), and the red blood cell count and hematocrit significantly decreased at 1 h after decompression (t=-2.606, -2.481; P=0.031, 0.038). After decompression, the platelet count first increased and then decreased, and the difference was significant (F=3.024, P=0.039); and the platelet count at 12 h after decompression was significantly higher than that before decompression (t=2.545, P=0.031). Conclusion We have successfully established a rabbit decompression sickness model and a set of evaluating parameter system considering the overall behavior, histopathology of lung and spinal cord tissues, inflammatory response and coagulation tests.