Objective: To evaluate the pathophysiology involved in hypocalcemia in septic shock and to investigate the value of calcium administration.
Design: Prospective, randomized placebo-controlled trial with parallel groups.
Setting: Animal research laboratory at the University Hospital of Uppsala.
Subjects: Twenty-four pigs aged 12-14 wks receiving general anesthesia.
Interventions: Twenty pigs received endotoxin infusion (10 microg/kg/hr) for 6 hrs. Ten of these pigs also received a calcium infusion (20 mmol total) in parallel. Four control pigs received only saline.
Measurements and main results: At the end of the study, blood ionized calcium (Ca2+) had declined from 1.32+/-0.04 mmol/L (mean +/- SD) to 1.09+/-0.06 mmol/L in pigs receiving endotoxin (p < .05 vs. controls) compared with 1.38+/-0.04 mmol/L to 1.25+/-0.07 mmol/L in controls and 1.39+/-0.03 mmol/L to 1.24+/-0.07 mmol/L in endotoxemic pigs receiving calcium. In both endotoxemic groups, total calcium levels in ascites were increased by 56% (p < .005 vs. controls), and an accumulation of calcium in the liver was mainly seen in the endotoxemic group receiving calcium (p < .008 vs. controls). Total Ca2+ levels in adiposal tissue and skeletal muscle were similar in all groups. Calcium administration did not significantly alter systemic hemodynamics or survival in this model of septic shock (four survivors in the endotoxemic group and five in the calcium administration group).
Conclusions: Endotoxemia in the pig rapidly induced hypocalcemia. Calcium accumulation was found in ascites and in the liver, but not in other examined tissues. Calcium administration, restoring the Ca2+ concentration, did not improve hemodynamics or survival in this model of hypodynamic sepsis. Porcine endotoxemic shock, which replicates human septic shock, seems to be suitable for evaluating calcium turnover.