Trauma may induce disturbance in the homeostasis and metabolism of phosphate. Serum phosphate decreases rapidly after trauma, and this rapid fall is followed by more slowly progressing hypophosphataemia, reaching minimum values on post-trauma days 2-5. The effect of propranolol on post-traumatic hypophosphataemia was studied in an experimental model, using anaesthetized pigs. Propranolol prevented the initial rapid decrease in serum phosphate. Twelve hours after the trauma, however, both the propranolol-treated and the untreated pigs showed significant serum phosphate depletion, with progression during the 48-hour observation period. The urinary phosphate excretion did not differ between the two groups, and after 48 hours the cumulative loss was the same in both groups. The adrenergic response to trauma was significantly greater in the propranolol-treated than in the untreated group. The results suggested that the rapid serum phosphate fall immediately after trauma was caused by adrenaline release. The second, slower phase was not related to adrenaline or noradrenaline release, but showed correlation with the urinary loss of phosphate.