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- Author or Editor: Jose C. Estepa x
- Clinical Pathology x
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Abstract
Objective—To establish reference values for protein-bound, ionized, and weak-acid complexed fractions of calcium and magnesium in equine serum and determine stability of ionized calcium (iCa) and ionized magnesium (iMg) in serum samples kept under various storage conditions.
Animals—28 clinically normal horses.
Procedure—Total calcium (tCa) and magnesium (tMg) in equine serum were fractionated by use of a micropartition system that allows separation of protein-bound calcium (pCa) and magnesium (pMg) and ultrafiltrable calcium (μCa) and magnesium (μMg) fractions. Serum concentrations of iCa and iMg were measured in the ultrafiltrate by use of selective electrodes. Serum concentration of complexed calcium (cCa) or magnesium (cMg) was calculated by subtracting iCa or iMg from μCa or μMg, respectively.
Results—Mean ±SE serum tCa concentration was 3.26 ± 0.06 mmol/L. Calcium fractions were as follows: pCa, 1.55 ± 0.03 mmol/L (47.4 ± 0.9%); iCa, 1.58 ± 0.03 mmol/L (48.5 ± 0.7%); and cCa, 0.13 ± 0.02 mmol/L (4.1 ± 0.9%). Serum tMg concentration was 0.99 ± 0.04 mmol/L. Magnesium fractions were as follows: pMg, 0.33 ± 0.04 mmol/L (33.3 ± 4.2%); iMg, 0.57 ± 0.02 mmol/L (57.6 ± 1.7%); and cMg, 0.09 ± 0.02 mmol/L (9.1 ± 1.9%). Refrigeration (4°C) did not affect iCa values, whereas iMg declined by 8% after 120 hours. Neither iCa nor iMg was affected by freezing (−20°C).
Conclusions and Clinical Relevance—In equine serum, iMg is less stable than iCa; thus, when serum samples are not going to be analyzed promptly, freezing may be preferable to refrigeration for storage.
Abstract
Objective—To evaluate the effects of metabolic acidosis and changes in ionized calcium (Ca2+) concentration on PaO2 in dogs.
Animals—33 anesthetized dogs receiving assisted ventilation.
Procedure—Normal acid-base status was maintained in 8 dogs (group I), and metabolic acidosis was induced in 25 dogs. For 60 minutes, normocalcemia was maintained in group I and 10 other dogs (group II), and 10 dogs were allowed to become hypercalcemic (group III); hypocalcemia was then induced in groups I and II. Groups II and IV (5 dogs) were treated identically except that, at 90 minutes, the latter underwent parathyroidectomy. At intervals, variables including PaO2, Ca2+ concentration, arterial blood pH (pHa), and systolic blood pressure were assessed.
Results—In group II, PaO2 increased from baseline value (96 ± 2 mm Hg) within 10 minutes (pHa, 7.33 ± 0.001); at 60 minutes (pHa, 7.21 ± 0.02), PaO2 was 108 ± 2 mm Hg. For the same pHa decrease, the PaO2 increase was less in group III. In group I, hypocalcemia caused PaO2 to progressively increase (from 95 ± 2 mm Hg to 104 ± 3 mm Hg), which correlated (r = −0.66) significantly with a decrease in systolic blood pressure (from 156 ± 9 mm Hg to 118 ± 10 mm Hg). Parathyroidectomy did not alter PaO2 values.
Conclusions and Clinical Relevance—Induction of hypocalcemia and metabolic acidosis each increased PaO2 in anesthetized dogs, whereas acidosis-induced hypercalcemia attenuated that increase. In anesthetized dogs, development of metabolic acidosis or hypocalcemia is likely to affect ventilatory control.
