Etomidate shortens the onset time of the neuromuscular block with vecuronium. This etomidate drug interactions enhances the bradycardia induced by vecuronium.
Miller’s anesthesia says the following about etomidate drug interactions –
The specific endocrine effects manifested by etomidate are a dose-dependent reversible inhibition of the enzyme 11β-hydroxylase, which converts 11-deoxycortisol to cortisol, and a relatively minor effect on 17α-hydroxylase .
This activity results in an increase in the cortisol precursors 11-deoxycortisol and 17-hydroxyprogesterone and an increase in ACTH. The blockade of 11β-hydroxylase and, to a lesser extent, 17α-hydroxylase seems to be related to the free imidazole radical of etomidate-binding cytochrome P-450.
This results in inhibition of ascorbic acid resynthesis, which is required for steroid production in humans. The blockade of the cytochrome P-450–dependent enzyme 11β-hydroxylase also results in decreased mineralocorticoid production and an increase in intermediaries (11-deoxycorticosterone).
Vitamin C supplementation restores cortisol levels to normal after the use of etomidate. Because minor adrenocortical suppressive effects were shown to follow even single bolus doses, concerns about the use of etomidate for anesthetic induction arose.
No large prospective studies have been done, but several smaller studies have provided some insight into the exact nature of adrenocortical suppression after an induction dose.