Mammary implants, diving, and altitude exposure.

Mammary implants were exposed to various simulated dive profiles followed by altitude exposures to stimulate aircraft travel and then were observed for bubble formation and volume changes. Minimal volume changes occurred after each dive. Numerous bubbles formed, however, reaching their maximum size in 3 hours. By comparison, when implants were exposed to high altitude following a dive exposure, significant volume changes occurred. This in vitro study showed that bubble formation and volume expansion occur after exposing implants to diving and altitude, but the circumstances required to produce these changes in vivo are extremely unlikely to occur normally.

Opposing effects of anesthetics on pressure tolerance and compression rate effect.

Inert gas narcotics increase intrinsic pressure tolerance (1,000Pc) in CD-1 mice but interfere with development of the protective responses raising seizure thresholds during slower compression (e.g., 60Pc). This secondary narcotic effect can block up to 40% of the total attainable increase in Pc. The narcosis susceptible moiety of this compression rate effect develops early, whereas a narcosis resistant remnant accounts for increase in Pc occurring after 90 min of compression or pressure exposure. Pressure conditioning by multiday pressure exposure entails increases in both 60Pc and 1,000Pc and in virtual annullment of the compression rate effect. The effect can be completely blocked by narcotic gases in the conditioning atmosphere. In addition to blocking part of the compression rate effect the presence of narcotic gases under these conditions can reverse the effects of previously established pressure conditioning. 60Pc regresses much more slowly under these conditions than 1,000Pc. Either reversal rate is much more rapid in air at 1 ATA than at 80 ATA under 0.9 atm N2O. The implications of these data are discussed with regard to evaluation of the hypothesis of antagonism between inert gas narcotics and high pressures and to elaboration of the monoamine hypothesis to account for the modification of the compression rate effect by narcotic gases.

Effect of habituation to subanesthetic N2 or N2O levels on pressure and anesthesia tolerance.

Exposure of CD-1 mice to subanesthetic partial pressures of N2O (0.5 atm) or N2 (10-20 atm) for periods up to 14 days results in up to 40% decreases in the mean threshold pressure eliciting type I high-pressure neurological syndrome (HPNS) seizures, and in increases up to 38% in the N2 partial pressure producing anesthesia. For all combinations of preexposure time, N2 partial pressure, as well as identity of the conditioning gas the relations between the convulsion threshold pressure (Pc) and the anesthesia N2 pressure (Pa) appear to be uniquely correlated by the equation Pa = 54.5 - 0.2(Pc - 60)1.2. The potency of N2O with respect to these habituation phenomena is between 28 and 33 times higher than that of N2, depending on the aspects compared. Evidence is presented indicating that after 14 days of habituation the animals have attained between 75 and 85% compensation for the anesthetic as well as the anticonvulsant effects of the conditioning gas. The bearing of the results on the problem of the nature of the antagonism between inert gas narcotic agents and high pressure and on the hypothesis that habituation tends toward restoration of isofluidity (or some analogous normalization process) are discussed.