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Thirty-three patients with major depressive illness received electroconvulsive therapy (ECT), and serum growth hormone (GH) levels were measured 30, min before and 1, 5, 15, 30 and 60 min after treatment. Six of the patients were studied 2 days before the first ECT (ECT-1) while receiving anaesthesia only. The anaesthesia given appeared to depress GH levels, which were significantly lower at 1 and 5 min after ECT than before treatment. When ECT was given there was a recovery of the GH level at 60 min, indicating a stimulatory effect of ECT on GH secretion. In 26 of the patients also investigated during the sixth and last ECT (ECT-6) in a series, no such recovery was observed. This may be due to changes in the sensitivity of intracerebral monoaminergic receptors in neurons controlling GH secretion from the pituitary gland. Since inhibition of GH secretion is mediated via beta-adrenergic pathways, the depression of GH secretion may be due to ECT-induced supersensitivity of postsynaptic beta-adrenergic receptors. In 27 of the patients serum somatomedin A, measured by radioreceptorassay (SMA-RRA), was analysed before ECT-1 and in 19 patients before ECT-6. In seven subjects the SMA-RRA was measured 30 min before and 1, 5, 15, 30, and 60 min after ECT-1. SMA-RRA levels were mainly within the normal range for age and did not change during ECT. No difference in SMA-RRA levels was observed before ECT-1 and ECT-6. This indicates that, although abnormalities in the GH-response to challenge stimuli have been reported in adults with major depressive disorder, their GH production is normal.
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