It was earlier demonstrated that the duration of tracheal noises of forced exhalation (FE) looks to be promising to determine adverse changes in the lung function after a dive. This study dealt with the param eters of tracheal expiratory noises (FE) as dependent of the composition of breathing gas mixtures. In the first type of experiments, 25 volunteers aged from 22 to 60 years carried out forced exhalation under a normal pres sure of air or of an oxygen-helium or oxygen-krypton mixture. In the second type of experiments, six vol unteers from 25 to 46 years of age performed forced exhalation with air in an altitude chamber under a normal pressure (0.1 MPa); the same subjects performed FE under an elevated pressure (0.263 MPa) while breathing air or an oxygen-helium mixture. In the first type of experiments, the total duration of tracheal FE noises in the frequency range 200-2000 Hz and 200 Hz bands FE noises depended directly and linearly on the density of the gas mixture; this was not the case in the high frequency band from 1400 to 2000 Hz. In the second type of experiments, the high frequency durations and spectral energies of tracheal FE noises (1600-2000 Hz) depended inversely and significantly on the adiabatic gas compressibility. In a simulated dive to a depth of 16.3 m (0.263 MPa), individual changes in the total duration of tracheal FE noises exceeded the diagnostic threshold of deterioration of the lung function in divers that was determined earlier under normal pressure.
The dynamics of changes in serum proteome was studied under conditions of experimental 9-day seclusion in a pressure chamber at 5 m H(2)O pressure with modified gaseous environment. The proteomic profile for the molecular weight range of 1000-17,000 Da changed by 75%. Increased content of acute phase proteins (complement components, inter-α-trypsin inhibitor, and high-molecular-weight kininogen) was observed on day 1 of the experiment before the exposure. On day 9 of exposure, the peaks of AII, CI, and CII apolipoproteins decreased and angiotensin II peak increased.
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