RESUMO
OBJECTIVE: It is suggested that one of the mechanisms for high pressure nervous syndrome (HPNS) is related to nervous cell membranous fluidity. Both pressure and fatty acid components of cell membranes would influence membrane fluidity. The present research probed into the relationship between different fatty acid components of brain cell membrane and individuals' degree of HPNS. METHODS: Four groups of mice were compressed to 4.1 MPa with an He-O2 mixture over a period of two hours. These animals had been fed with different diets for a period of months prior to the procedure. We recorded interpeak latency of Wave 1 to Wave 4 (IPL1-4) of brainstem auditory-evoked potential (BAEP) at different stages of compression. Animals were sacrificed immediately after surfacing. Both polyunsaturated fatty acids (PUFAs) and saturated fatty acids (SFAs) of brain cell membranes were analyzed by HPLC. RESULTS: Upon arriving at 4 MPa, the IPL1-4 readings of the four groups were prolonged 0.294 +/- 0.400 milliseconds (ms), 0.156 +/- 0.200 ms, 0.009 +/- 0.182 ms and 0.025 +/- 0.137 ms separately; each corresponded to its own PUFA-percent constitution of 16.2 +/- 4.5%, 24.8 +/- 4.3%, 33.5 +/- 8.8% and 32.3 +/- 2.9% respectively on the basis of total fatty acids. DISCUSSION AND CONCLUSION: Varying fractions of PUFAs, implying different membrane fluidity, interfered with disturbance of synaptic transmission during hyperbaric exposure. In other words, the higher the ratio of PUFAs/SFAs to the brain cell membrane, the stronger the ability for animals to antagonize the pressure effect.
