The sudden death was induced by an intravenous injection of KCl and succinylcholine chloride (SCC). The agony period was the time from the administration of the substance to final cardiac arrest. In both sexes, the immunoreactive-beta-endorphin level was significantly lower in respiratory failure than in cardiac failure. No variation in plasma immunoreactive-beta-endorphin was noted during short periods of agony in cardiac failure, but it markedly increased during long periods of agony in respiratory failure. The highest elevation at 2 or 4 minutes after SCC administration was about 3 times the pre-administration value for immunoreactive-beta-endorphin in males. But elevation in females was lower than in males. The rise in the plasma beta-endorphin during the agony of sudden death from respiratory failure is regarded to be of pituitary origin due to dexamethasone treatment. Results indicated that the pituitary responded more to the fatal agony in respiratory failure than in cardiac failure. Tables, figures, and 13 references (Author abstract modified)