Effects of the synthetic estrogen 17 alpha-ethinylestradiol on the life-cycle of the fathead minnow (Pimephales promelas).

A fish full life-cycle (FFLC) study was conducted for 17 alpha-ethinylestradiol (EE2) using the fathead minnow, Pimephales promelas. Newly fertilized embryos (< 24 h old) were exposed to five concentrations of EE2 (0.2, 1.0, 4.0, 16, and 64 ng/L nominal) in continuous flow-through conditions for 305 d at 25 +/- 1 degrees C. Exposure concentrations were verified by 14C-EE2 radiochemistry, supported by radioimmunoassay, and mean measured values were > or = 70% of nominal. For the F0 adult phase until 301 d posthatch, the no-observed-effect concentrations (NOECs) for growth, survival, and reproduction (as egg production) were all > or = 1.0 ng/L. The NOEC values for F1 embryo hatching success and larval survival (at 28 d posthatch) were both > or = 1.0 ng/L. While statistically detectable changes in F1 growth were evident at 0.2 ng/L, these were not considered to be biologically significant when compared with historical control data. Male fish exposed to EE2 at 4.0 ng/L failed to develop normal secondary sexual characteristics; on the other hand, assumed females exposed to this level of EE2 were able to breed when paired with males that had not been exposed to EE2. Histology of F0 control, 0.2-, and 1-ng/L exposed fish at 56 d posthatch indicated an approximate female-to-male (F:M) sex ratio of 50:50 (with no ovatestes observed in the control), while fish exposed to EE2 at 4.0 ng/L for 56 d posthatch had a F:M sex ratio of 84:5 (with ovatestes in 11% of fish). After 172 d posthatch, no testicular tissue was observed in any fish exposed to EE2 at 4.0 ng/L. At the same time point, plasma vitellogenin levels were significantly higher in fish exposed to EE2 at 16 ng/L. A lack of sexual differentiation occurred in males at concentrations > or = 4.0 ng/L. Taking into account these data, the overall no-observed-adverse-effect concentration was considered to be 1.0 ng/L.

Application of the mechanical oscillator technique to the investigation of EVA decompression.

The ultrasonic bubble detection technique has been used as a versatile tool in the investigation of hypobaric decompression procedures for the last two decades. However, this method can only detect relatively large bubbles > 30-50 micrometers (usually in venous blood) and not the very first stages of bubble formation. Recently, the mechanical oscillator technique has been applied in air diving trials in order to detect small blood density changes due to hypothetical fluid shifts. However, sharp density drops were found in the decompression process, and these have been attributed to gas bubble formation. In this study, this method was applied together with Doppler controls to a series of altitude decompressions to 300 and 500 hPa, which represents the range of EVA operational pressures currently used or planned. Six subjects participated in both series; the oscillator sample tube could be pressurized. By the application of pressure on a blood sample containing questionable gas bubbles, these are reduced in volume, like in recompression therapy, and thus the density of the sample is increased. This effect has been shown in all 6 subjects undergoing decompression to 300 hPa, whereas in the 500 hPa series only 3 out of 6 subjects corresponded with gas phase formation immediately after decompression. Typically, Doppler bubbles appeared only after some latency time between 20 and 60 min; after this time, the density effect had nearly vanished. It is concluded that the mechanical oscillator technique represents a complementary research instrument to the Doppler method, because it is able to deliver a quantitative resolution of the early stage of gas phase formation.

Human brainstem auditory-evoked potentials in deep experimental diving to pressures up to 62.5 bar.

The neural mechanisms underlying the high pressure neurologic syndrome (HPNS), which limit man's safe advance to extreme diving depths, are still unclear. This work was aimed at a better understanding of HPNS through study of brainstem auditory-evoked potentials (BAEP). BAEP were repeatedly recorded within 2 experimental chamber dives, Titan VIII (2 divers, maximum depth of 560 msw, compression time to bottom 109 h) and Titan XI (3 divers, maximum depth of 615 msw, compression time to bottom 240 h). Prolongation of the IV/V-complex occurred in 2 divers upon reaching 525 msw during Titan VIII compression and was accompanied by vestibular disturbances and amplitude increases of finger tremor. Both categories of changes--clinical signs and IV/V delay--gradually diminished during a 4-day stay at 545 msw, suggesting that they depended on excessive compression rates and insufficient acclimation time. Longer holding times at intermittent depths during Titan XI clearly reduced both HPNS symptoms and magnitude of prolongation of IV/V latencies. Wave I and wave III latency did not significantly change, pointing to a suppression of pontomesencephalic transmission. We infer that pressure suppresses synaptic transmission or triggers an increase of cortical or subcortical efferent inhibitory modulation of upper pontine and midbrain auditory afferents. Postdive controls revealed no persistent changes of BAEP measures in either the Titan VIII or XI divers.

Nitrogen partial pressures in man after decompression from simulated scuba dives at rest and during exercise.

In 5 subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure to air at 6 bar for 30 min corresponding to a depth of 50 m. Afterward the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6, and 1.3 bar with a total decompression time of 67 min. In 3 of the subjects the measurements were repeated after they had exercised (workload 75 W) during bottom time. Immediately after decompression and every 40 min until Minute 240 arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min after decompression, indicating still incomplete nitrogen washout for at least 2 h after decompression had been accomplished. We did not find any difference in PN2 values after decompression from dives at rest and after exercise. Applying a computer program based on a wide range of theoretical tissue half-times nitrogen elimination proved to be consistent with Haldanian theories when using our decompression profile. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest and after exercise.