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The present study provides systematic evidence indicating a direct relationship between environmental temperature, rectal temperature and ethanol lethality. Male, C57 BL/6J mice, previously housed at room temperature (23 +/- 1 degree C), were injected intraperitoneally with 4.8 to 9.2 g kg-1 ethanol and then exposed for 24 h to ambient temperatures that did not appreciably exceed the thermally neutral range for sober mice (20 to 35 degrees C). There was a direct relationship between temperature and ethanol lethality at 8 and 24 h after injection. The 8 h LD50 increased by 64%, from 5.3 to 8.7 g kg-1, as environmental temperature decreased from 35 to 20 degrees C. The 24 h LD50 increased by 51%, from 5.3 to 8.0 g kg-1, across this temperature range. Each 5 degrees C reduction in ambient temperature induced a significant decrease in the rectal temperature of ethanol-injected mice. Mean rectal temperature ranged from 2.2 degrees C above baseline at an ambient temperature of 35 to 15 degrees C below baseline in the 20 degrees C environment. Ethanol induced a significant dose-related hypothermia in mice exposed to the 20, 25 and 30 degrees C environments but did not produce hypothermia in animals kept in the 35 degrees C environment. These findings indicate that the potency of potentially lethal ethanol doses varies with body temperature in accordance with partition and membrane expansion-fluidization theories of anaesthesia.

Dose- and pressure-related interactions between ethanol anesthesia and low-level hyperbaric helium-oxygen environments were studied in mice using conditions which eliminated the possibility of hypoxia during compression and hyperbaric helium-induced hypothermia. Hyperbaric helium-oxygen (1–12 atmospheres absolute) reduced sleep time in a pressure-related manner. The degree of maximum ethanol antagonism decreased as the ethanol dose increased (3.2, 3.6, and 4.0g/kg). The results are consistent with membrane theories of general anesthesia and suggest a possible common mechanism between ethanol antagonism at low hyperbaric pressure and high-pressure reversal of anesthesia.

Male and female C57BL/6J and male BALBc/J mice were injected with 3.6 g/kg ethanol or saline and exposed to 1-10 atmospheres absolute (ATA) air, to 1 ATA 80% helium-20% oxygen, or to 12 ATA helium-oxygen having oxygen partial pressures between 0.5 and 18 times normal. Hyperbaric helium-oxygen significantly reduced sleep-time and increased wake-up brain ethanol concentrations in all mice tested. The degree of antagonism was not enhanced by increasing the oxygen partial pressure. Hyperbaric air increased sleep-time and decreased wake-up brain ethanol concentration in C57 mice. Hyperbaric air induced a pressure-related lethal effect beginning at 6 ATA in intoxicated BALBs. These findings demonstrate that hyperbaric ethanol antagonism extends across strains and sexes, that the degree of antagonism cannot be enhanced by increasing the oxygen partial pressure, and that air is not suitable as an antagonistic hyperbaric gas. The findings are consistent with membrane theories of anesthesia.

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