Three minutes after dexmedetomidine administration (Fig. 2A), SaO 2 decreased from 95.75% ± 0.46-62.89% ± 2.83%, representing a decrease of 65.68% from baseline. SaO 2 recovered to 77.19% ± 3.91% at 33 minutes (80.62% of baseline). Dexmedetomidine decreased SaO 2 from 95.78% ± 0.30-84.51% ± 3.10% at 3 minutes ( Φ P < 0.0001) (88.23% of baseline). SaO 2 recovered to 81.89% ± 3.46% at 33 minutes (85.50% of baseline). There was no signi cant change in SaO 2 after administration of 8 mg/kg tandospirone. Compared with the vehicle control group, pre-injection of WAY100635 completely blocked the ability of tandospirone to improve respiratory depression (Fig. 2B). A 6-minute baseline measurement was made prior to the experiment. A considerable reduction in SaO 2 was recorded 6 minutes after atipamezole injection in all groups (Fig. 2C), implying that the model of respiratory depression was compared by two-way analysis of variance (dose × time) followed by Bonferroni's post hoc test. The data are expressed as the mean ± standard error of the mean. * P < 0.05 was considered statistically signi cant. pro ciently established. The experimental results demonstrate that atipamezole blocked respiratory depression caused by dexmedetomidine.