Posttraumatic hypophosphataemia and urinary phosphate excretion with and without phosphate supplementation. An experimental study in pigs.
Hypophosphataemia commonly follows trauma of various types. Several aetiologic factors have been proposed and the clinical significance of posttraumatic hypophosphataemia has been discussed. For study of the mechanisms underlying hypophosphataemia associated with surgical trauma, an experimental model has been developed which permits induction of hypophosphataemia under standardized conditions in anaesthetized and traumatized pigs. In the present study this model was used to investigate the relationship between posttraumatic hypophosphataemia and urinary excretion of with or without phosphate supplementation. The results suggest that the adrenaline release associated with stress and trauma induced an immediate and rapid fall in the serum phosphate (S-P) level. The abrupt fall was followed after 24 hours by a slower decrease. This second phase of S-P decrease was not induced by catecholamine release or by glucose infusion and was not prevented by phosphate supplementation. It appeared to be related to an inadequate renal response to the hypophosphataemia, i.e. a relative phosphaturia. The cause of this phosphaturia is not fully understood, but both extracellular volume expansion and the humoral response to trauma are possible explanations.
D000818:Animals; D004573:Electrolytes / Q000097:blood; D004837:Epinephrine / Q000097:blood; D004911:Erythrocyte Volume / Q000187:drug effects; D005260:Female; D008297:Male; D009638:Norepinephrine / Q000032:analysis; D010710:Phosphates / Q000008:administration & dosage / Q000097:blood* / Q000652:urine; D013552:Swine; D014947:Wounds and Injuries / Q000150:complications*
D004573:Electrolytes; D010710:Phosphates; D009638:Norepinephrine; D004837:Epinephrine