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Keywords:

  • Animal model;
  • Calcium;
  • Magnesium;
  • Parathyroid hormone;
  • Sepsis;
  • Vitamin D

Background

Hypocalcemia is a documented electrolyte disturbance in people and animals with sepsis, but its mechanism is poorly understood.

Objective

To investigate mechanisms of hypocalcemia in dogs with experimentally induced endotoxemia.

Animals

Six healthy mixed breed dogs were included in this nonrandomized, placebo-controlled, crossover study.

Methods

Dogs initially were injected with placebo (0.9% NaCl; 1 mL, IV) and then lipopolysaccharide (LPS; 2 μg/kg, IV) after a 5-day washout period. Blood and urine samples were collected for measurement of serum total calcium (tCa), ionized calcium (iCa), total magnesium (tMg), ionized magnesium (iMg), parathyroid hormone (PTH), 25-hydroxyvitamin D (vitamin D), venous blood gases, and fractional excretion (FE) of calcium.

Results

After LPS administration, body temperature increased and blood pressure decreased. Both iCa and tCa decreased (< .01), but iMg was not significantly different between control and LPS treatments. PTH concentrations increased (< .01) and vitamin D concentrations decreased (< .01). Venous pH, bicarbonate, base excess, and blood glucose also decreased (< .01). Urine tCa concentration was below the limit of detection for all dogs after LPS administration.

Conclusions

Hypocalcemia occurs during endotoxemia in dogs and is associated with hypovitaminosis D. Hypomagnesemia, hypoparathyroidism, alkalosis, and increased calciuresis are not associated with hypocalcemia in endotoxemic dogs.