| Summary: | Objective To explore the effect of general anesthetic, etomidate, on the expression of connexons in neurons induced by P19 cells, and illustrate the molecular mechanism of patients' consciousness loss after etomidate administration by means of immunocytochemistry. Methods The P19 cells were retro ⁃ induced to stem cells, which were then oriented ⁃ induced to neurons to receive neuron identification. The neurons were then allocated into group E (etomidate), group CAR (carbenoxolone), group LE (lipid emulsion) and group CON (phosphate buffer solution, control). Agents administrated respectively were withdrawn in 30 s, 60 min and 120 min, and connexin36 (Cx36) were counted through inference of immunocytochemistry. Results Cx36 were more suppressed for group E and group CAR than group CON in 30 s and 60 min (30 s: t = ⁃ 50.423, P = 0.000; 60 min: t = ⁃ 25.826, P = 0.000). As for the inner group analysis, group E and group CAR bared declined suppressive effects with even no statistic variance in 120 min compared to the respective untreated time points; as for group LE and group CON, no statistic variance existed between different times. Intergroup analysis showed that significant suppressive effects in 30 s were seen in group E and group CAR which were more than group LE and group CON (P < 0.05, for all) while the difference of suppressive effects were not seen between group E and group CAR (P > 0.05). In 60 min, positive ⁃ stained connexons were more suppressed in group E than in group CAR (t = ⁃ 2.782, P = 0.008). Etomidate gave more suppression than carbenoxolone and this stronger effect was not shown until 60 min. Conclusion Etomidate depresses the gap junction intercellular connection (GJIC) by means of decreasing the number of neuron connexons, which might be the molecular mechanism for patients' consciousness loss after etomidate administration.
DOI：10.3969/j.issn.1672-6731.2010.04.015
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