Background: To investigate the effects of unsafe decompression on rat pulmonary endothelial function and its relevant mechanisms.Methods: 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 k Pa compressed air environment for 60 min, and the pressure was then reduced by 100 k Pa/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(e NOS) 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: 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 e NOS expression between the DCS group and the control group was statistically insignificant(P>0.05), but the ratio of e NOS 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: Unsafe decompression during a simulated submarine escape process can lead to e NOS dimer uncoupling in the pulmonary artery endothelium. The dissociated e NOS monomer cannot synthesize nitric oxide(NO) and thus affect the endothelium-dependent vasodilation capacity. The e NOS 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 e NOS monomer can also cause an increase in the formation of ROS and thus mediate peroxidation damage. Background: To investigate the effects of unsafe decompression on rat pulmonary endothelial function and its relevant mechanisms. Methods: Sixty male Sprague-Dawley (SD) rats were randomly divided into a control group (n = 30) and a decompression sickness (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 k Pa compressed air environment for 60 min, and the pressure was then reduced by 100 k Pa / 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 (e NOS) in pulmonary artery tissues and all protein nitration levels in pulmonary artery tissues; reactive oxygen species (ROS) formation was measured via Results: 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). In vitro pulmonary artery superoxide anion probe dihydroethidium (DHE) . The difference in e NOS expression between the DCS group and the control group was statistically insignificant (P> 0.05), but the ratio of e NOS monomer / dimer in the DCS group was significantly higher than that in the control group (P <0.05 ). All results of DHE staining showed that the amount of ROS formation in the pulmonary arteries of the DCS group were significantly higher than those of the control group (P <0.05) group was significantly higher than that of the control group (P <0.05) .Conclusion: Unsafe decompression during a simulated submarine escape process can lead to e NOS dimer uncoupling in the pulmonary artery endothelium. The dissociated e NOS monomer can not synthesize nitric oxide (NO) and thus affect the endothelium-dependent vasodilation capacity. The e NOS 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 so mediate peroxidation damage.