Prevention of the Cardiovascular and Neuroendocrine Response to Electroconvulsive Therapy: 11. Effects of Pretreatment Regimens on Catecholamines, ACTH, Vasopressin, and Cortisol Matthew B. Weinger, MD, Brian L. Partridge, MD, DPhil, Richard Hauger, MD, Arvin Mirow, MD, and Marvin Brown, MD Departments of Anesthesiology, Psychiatry, and Medicine, University of California, San Diego, and Department of Veterans Affairs Medical Center, San Diego, California The neuroendocrine response to electroconvulsive therapy (ECT) was assessed in four patients after pretreatment with esmolol (1.0 mgkg), fentanyl (1.5 pg/kg), labetalol (0.3 mg/kg), and saline solution (control). Each patient received each drug pretreat- ment using a double-blind, randomized study block- design. During each of the five studies, blood sam- ples were obtained from each patient before anesthetic induction, before ECT shock, and at 1, zyxwvu 5, 10, and 30 min after seizure. Samples were subse- quently 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 epineph- rine levels, respectively zyxwvutsrq (P zyxwvutsrq < 0.05). The ACTH and cortisol levels gradually increased over 30 min, peak- ing at values that were two to three times the control values (P < 0.05). The AVP levels increased signifi- cantly after induction of ECT (P < 0.005) and re- mained higher than control levels at zyx 5, 10, and 30 min. The effect of pretreatments varied. Pretreat- ment with esmolol and fentanyl resulted in signifi- cant attenuation of the norepinephrine peak after seizure (P < 0.05). Only esmolol significantly atten- uated ECT-induced epinephrine secretion, whereas fentanyl pretreatment significantly reduced release of ACTH after ECT. No pretreatment significantly af- fected the elevated AVP or cortisol levels seen on emergence or up to 30 min after treatment. The ability of esmolol pretreatment to attenuate serum catechol- amine release after ECT is consistent with its ability to block the cardiovascular responses to ECT. (Anesth Analg 1991;73:56>9) lectroconvulsive therapy (ECT) is a frequently used therapy for patients with major affective E disorders but may have significant cardiovas- cular morbidity (1). In our accompanying paper (2), it was demonstrated that esmolol and labetalol signifi- cantly attenuated the cardiovascular response to ECT. The mechanism by which ECT produces tachy- cardia and hypertension remains to be fully eluci- dated. Previous studies have measured catechol- amine (3,4) and stress hormone (5) release after ECT. However, the effect on neuroendocrine release of Supported by Clinical Investigator and Research Associate Career Development Awards (R.H.) and Merit Review Grants (M.B.W., R.H., B.L.P.) from the Veterans Administration Medical Center and by NIH grant HL43154 (M.B.) and Pfizer Scholars Award (R.H.). Accepted for publication June 28, 1991. Address correspondence to Dr. Weinger, VA Medical Center (125), 3350 La Jolla Village Drive, San Diego, CA 92161. administering pretreatment drugs to blunt the cardio- vascular response to ECT has not been examined. The purpose of this study was to compare, using a double-blind, randomized, placebo-controlled, cross- over design, three previously advocated pretreat- ment regimens (esmolol, fentanyl, and labetalol)with saline controls with respect to their effects on serum catecholamines (epinephrine and norepinephrine) and on three markers of the stress response (adreno- corticotrophic hormone [ACTH], arginine vasopres- sin [AVP], and cortisol) and to correlate these neuro- endocrine effects with the hemodynamic response to ECT. Methods After Human Subjects Committee approval and pa- tients’ informed consent had been obtained and simultaneously with part I of this study (2), five of the 01591 by the International Anesthesia Research Society zyxwvutsrq 0003-2999/91/$3.50 Anesth Analg 1991;73:56>9 zy 563