Background:

2

To investigate the effects of unsafe decompression on rat pulmonary endothelial function and its relevant mechanisms.

Methods:

2

Sixty male Sprague-Dawley (SD) rats were randomly divided into a control group (n=30) and a decompression sickness (DCS) group (n=30). The DCS model was established by placing the rats in the DCS group in a pressurized cabin where they were exposed to a 600 kPa compressed air environment for 60 min

and the pressure was then reduced by 100 kPa/min until it reached atmospheric pressure. After the surviving rats in the DCS group and the rats in the control group were anesthetized

their pulmonary arteries were stripped to test the in vitro pulmonary artery endothelium-dependent vasodilation capacity. Western blotting was used to measure the expression and dissociation of endothelial nitric oxide synthase (eNOS) in pulmonary artery tissues and all protein nitration levels in pulmonary artery tissues; reactive oxygen species (ROS) formation was measured via in vitro pulmonary artery superoxide anion probe dihydroethidium (DHE) staining.

Results:

2

After experiencing unsafe decompression

10 of the 30 rats in the DCS group died. The pulmonary artery endothelium-dependent vasodilation capacity in the surviving rats decreased significantly (P<0.05). The difference in eNOS expression between the DCS group and the control group was statistically insignificant (P>0.05)

but the ratio of eNOS monomer/dimer in the DCS group was significantly higher than that in the control group (P<0.05). All protein tyrosine nitration levels in the pulmonary artery tissues of the DCS group were significantly higher than those of the control group (P<0.05). The results of DHE staining showed that the amount of ROS formation in the pulmonary arteries of the DCS group was significantly higher than that of the control group (P<0.05).

Conclusion:

2

Unsafe decompression during a simulated submarine escape process can lead to eNOS dimer uncoupling in the pulmonary artery endothelium. The dissociated eNOS monomer cannot synthesize nitric oxide (NO) and thus affect the endothelium-dependent vasodilation capacity. The eNOS monomer can promote peroxynitrite (ONOO

–

) synthesis

leading to an increase in protein tyrosine nitration levels in pulmonary artery tissues and causing disorder in cell cycle regulation. The eNOS monomer can also cause an increase in the formation of ROS and thus mediate peroxidation damage.