ABSTRACT
Objective To explore the effects of unsafe decompression on the endothelial function of pulmonary artery in rat and its possible related mechanism. Methods Sixty male SD rats (260±35g) were randomly divided into two groups (30 each): control group and decompression (DCS) group. Decompression sickness (DCS) model was reproduced by placing the rats in a compression chamber with air pressure of 600kPa for 60min, followed by decompression at a rate of 100kPa/min to normal pressure. The surviving rats in both control and DCS groups were sacrificed and their pulmonary artery was harvested. The endothelium dependent vasodilatation capacity of isolated pulmonary artery was assessed. The expression and uncoupling of endothelial nitric oxide synthetase (eNOS), as well as the nitration level of each kind of protein in the pulmonary artery tissue, were analyzed by Western blotting. The concentration of reactive oxygen species (ROS) in the pulmonary artery was determined with superoxide anion probe dihematoporphyrin ether (DHE) staining. Results Ten of 30 rats in DC group died of unsafe decompression, and the endothelium dependent vasodilatation capacity of excised pulmonary artery in survived rats was found to decline obviously (P0.05), but the ratio of eNOS monomer/dimer increased significantly in DC group than in control group (P<0.05). The tyrosine nitration level of each kind of protein in the pulmonary artery tissues was higher significantly in DC group than that in control group (P<0.05). DHE showed that the generated amount of DCS in pulmonary artery tissues was obviously higher in DC group than in control group (P<0.05). Conclusions Unsafe decompression may lead to uncoupling of eNOS dimers in the endothelium of pulmonary artery. Uncoupled eNOS monomers may inhibit the synthesis of NO, thereby affect the endothelium dependent vasodilatation function. On the other hand, the eNOS monomers may facilitate the anabolism of ONOO-, leading to an increase in tyrosine nitration level of each kind of protein in the pulmonary artery tissues, thereby cause the regulation disorder of cell information system. The eNOS monomers may also increase the production of ROC, there by mediate the peroxide injuries.
ABSTRACT
21 male adult goats were divided into the experimental group (11 goats) and control group (10 goats). The pressure-time of hyperbaric pretreatment was 700kPa-3min. The rates of the compressions and decompressions of hyperbaric pretreatments were l00kPa/min. The intervals between hyperbaric pretreatments and simulated divings which were repidly decompressed were 15min. The pressure-time of simulated diving was 600 kPa-60min. The rates of the compressions of the simulated divings were l00kPa/min and those of the decompressions were 60kPa/min. The results indicated that hyperbaric pretreatments might reduce the bubble formation and increased 5-HT concentrations which were caused by rapid decompression after simulated divings, and that other indexes such as morbility and mortality of decompression disease, platelet count of circulation, and bubble sound of blood flow on the precardium of the goats changed coincidently. These suggest that hyperbaric pretreatments could prevent goat's experimental decompression disease in some degree.