Prevention of the cardiovascular and neuroendocrine response to electroconvulsive therapy: II. Effects of pretreatment regimens on catecholamines, ACTH, vasopressin, and cortisol.

The neuroendocrine response to electroconvulsive therapy (ECT) was assessed in four patients after pretreatment with esmolol (1.0 mg/kg), fentanyl (1.5 micrograms/kg), labetalol (0.3 mg/kg), and saline solution (control). Each patient received each drug pretreatment using a double-blind, randomized study block-design. During each of the five studies, blood samples were obtained from each patient before anesthetic induction, before ECT shock, and at 1, 5, 10, and 30 min after seizure. Samples were subsequently analyzed for epinephrine, norepinephrine, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), and cortisol. Electroconvulsive therapy after saline pretreatment resulted in a 3-fold and 15-fold increase in norepinephrine and epinephrine levels, respectively (P less than 0.05). The ACTH and cortisol levels gradually increased over 30 min, peaking at values that were two to three times the control values (P less than 0.05). The AVP levels increased significantly after induction of ECT (P less than 0.005) and remained higher than control levels at 5, 10, and 30 min. The effect of pretreatments varied. Pretreatment with esmolol and fentanyl resulted in significant attenuation of the norepinephrine peak after seizure (P less than 0.05). Only esmolol significantly attenuated ECT-induced epinephrine secretion, whereas fentanyl pretreatment significantly reduced release of ACTH after ECT. No pretreatment significantly affected the elevated AVP or cortisol levels seen on emergence or up to 30 min after treatment. The ability of esmolol pretreatment to attenuate serum catecholamine release after ECT is consistent with its ability to block the cardiovascular responses to ECT.