Background: We examined the effects of etomidate on recovery of contractile function after hypoxia reoxygenation and hypoxic preconditioning in vitro using isolated human myocardium.
Methods: Human right atrial myocardium were obtained at the time of cardiac surgery from 38 adults patients. We recorded isometric force of contraction (FoC) of atrial trabeculae suspended in an oxygenated Tyrode's solution (34 degrees C, stimulation frequency 1 Hz). In all groups, a 30-min hypoxic period was followed by 60 min of reoxygenation (HR). In separate groups, muscles were exposed to etomidate (10(-7), 10(-6), 10(-5) M) 10 min before and throughout the HR periods. Hypoxic preconditioning was induced by 4-min hypoxia followed by 7-min reoxygenation applied before HR periods. Etomidate 10(-5) M was administered before, throughout, and after the hypoxic preconditioning stimulus. Recovery of FoC (expressed as % of baseline value) at the end of HR was compared among groups.
Results: Compared with the control group (FoC: 52%+/-10%), etomidate 10(-7) M (FoC: 57%+/-9%; P=0.24), 10(-6) M (FoC: 61%+/-11%; P=0.10), and 10(-5) M (FoC: 54%+/-9%; P=0.29) did not modify the recovery of FoC after HR. Hypoxic preconditioning-induced increase in the recovery of FoC (87%+/-5%; P<0.001 vs control group) was not modified in the presence of etomidate 10(-5) M (FoC: 86%+/-7%; P=0.74 vs hypoxic preconditioning group).
Conclusions: Etomidate did not modify the in vitro FoC of human myocardium exposed to HR. Furthermore, etomidate did not modify the protective effect of hypoxic preconditioning.