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Changes in a hexobarbital anaesthesia threshold in rats induced by repeated long-term treatment with barbital or ethanol

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Abstract

The quantity of intravenously infused hexobarbital needed to produce a burst suppression of 1 sec or more in the EEG was determined in male rats after chronic barbital or ethanol treatments. The ensuing “sleeping times” were also recorded.

At the end of the first treatment with barbital (200 mg/kg/day i.p. for 5 weeks) the hexobarbital thresholds had increased by approximately 45% compared with a pre-experimental average. The thresholds were back to normal after approximately a week. At the end of a second treatment with barbital there was a similar, slightly more prolonged, immediate increase in threshold. Three weeks after the second treatment there was also a new increase in threshold (Figs. 2 and 3). The ensuing “sleeping times” were unaffected.

Ethanol treatment (10% W/V in the drinking water allowed twice 1 h each day for 16 weeks) caused a gradual increase in threshold which reached a maximum (20%) around day 9–10 after the end of the treatment (Fig.5). Two weeks after the ethanol treatment the thresholds were essentially normal. In an earlier barbital treated (200 mg/kg/day i.p. for 5 weeks) group a second slightly larger increase was also seen around 3 weeks after the end of the ethanol treatment. In this group an increase was also seen in the ensuing “sleeping times” but this increase seemed to be unrelated to the increases in threshold.

These late changes in threshold after a second treatment seem to be due to a “summation” of changes induced by the two treatments. In this respect ethanol and barbital are probably related. They are, however, not identical with respect to their effects on the hexobarbital threshold after interruption of chronic treatment. This is shown by the longer latency of the immediate changes after ethanol treatments.

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Wahlström, G. Changes in a hexobarbital anaesthesia threshold in rats induced by repeated long-term treatment with barbital or ethanol. Psychopharmacologia 19, 366–380 (1971). https://doi.org/10.1007/BF00404381

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