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- Author or Editor: Ignacio Lopez x
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Objective—To characterize the dynamics of calcitonin secretion in response to experimentally induced hypercalcemia in cats.
Animals—13 healthy adult European Shorthair cats.
Procedures—For each cat, the calcitonin response to hypercalcemia (defined as an increase in ionized calcium concentration > 0.3mM) was investigated by infusing calcium chloride solution and measuring circulating calcitonin concentrations before infusion (baseline) and at various ionized calcium concentrations. Calcitonin expression in the thyroid glands of 10 of the cats was investigated by immunohistochemical analysis.
Results—Preinfusion baseline plasma calcitonin concentrations were very low in many cats, sometimes less than the limit of detection of the assay. Cats had a heterogeneous calcitonin response to hypercalcemia. Calcitonin concentrations only increased in response to hypercalcemia in 6 of 13 cats; in those cats, the increase in calcitonin concentration was quite variable. In cats that responded to hypercalcemia, calcitonin concentration increased from 1.3 ± 0.3 pg/mL at baseline ionized calcium concentration to a maximum of 21.2 ± 8.4 pg/mL at an ionized calcium concentration of 1.60mM. Cats that did not respond to hypercalcemia had a flat calcitonin-to-ionized calcium concentration curve that was not modified by changes in ionized calcium concentration. A significant strong correlation (r = 0.813) was found between the number of calcitonin-positive cells in the thyroid gland and plasma calcitonin concentrations during hypercalcemia.
Conclusions and Clinical Relevance—Healthy cats had very low baseline plasma calcitonin concentrations. A heterogeneous increase in plasma calcitonin concentration in response to hypercalcemia, which correlated with the expression of calcitonin-producing cells in the thyroid, was identified in cats.
Objective—To provide reference values for serum biochemical variables that are used for evaluation of mineral metabolism in donkeys and compare values with those in horses.
Animals—18 donkeys and 18 horses.
Procedures—Total calcium (tCa), total magnesium (tMg), and inorganic phosphorus (P) concentrations were measured in serum samples via spectrophotometry. Ionized calcium (iCa) and magnesium (iMg) concentrations were quantified with selective electrodes. By use of a micropartition system, tCa and tMg were fractionated to separate protein-bound (pCa, pMg) and ultrafiltrable fractions. Complexed calcium (cCa) and magnesium (cMg) concentrations were calculated by substracting ionized fractions from ultrafiltrable fractions. Parathyroid hormone (PTH) and calcitriol (CTR) concentrations were measured via radioimmunoassay.
Results—Serum tCa concentration in donkeys (3.37 ± 0.21 mmol/L) was composed of pCa (1.59 ± 0.21 mmol/L [47.0 ± 4.2%]), iCa (1.69 ± 0.04 mmol/L [50.4 ± 3.0%]), and cCa (0.09 ± 0.08 mmol/L [2.6 ± 2.9%]). Serum tMg concentration (1.00 ± 0.08 mmol/L) was fractioned in pMg (0.23 ± 0.08 mmol/L [23.4 ± 8.1%]), iMg (0.59 ± 0.04 mmol/L [58.8 ± 5.1%]), and cMg (0.18 ± 0.08 mmol/L [17.8 ± 7.2%]). Serum concentrations of P (1.14 ± 0.30 mmol/L), PTH (20.4 ± 21.2 pg/mL), and CTR (13.4 ± 5.9 pg/mL) were determined.
Conclusions and Clinical Relevance—Serum variables of mineral metabolism in donkeys were within reference ranges for horses. However, when compared with horses, donkeys had higher iCa, cMg, and CTR and lower pMg and PTH concentrations.
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.
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.
Objective—To evaluate changes in plasma ionized calcium (Ca2+) and parathyroid hormone (PTH) concentrations in horses competing in endurance rides.
Design—Longitudinal clinical study.
Procedure—Venous blood samples were obtained from horses before and after racing 80 km. Plasma pH and concentrations of Ca2+, PTH, inorganic phosphorus, albumin, lactate, and magnesium were measured.
Results—Overall, a significant decrease in mean (± SD) plasma Ca2+ concentration (from 6.44 ± 0.42 to 5.64 ± 0.42 mg/dl) and a significant increase in plasma PTH concentration (from 49.9 ± 30.1 to 148.1 ± 183.0 pg/ml) were found after exercise. Exercise also resulted in significant increases in plasma inorganic phosphorus, albumin, and lactate concentrations. No changes in plasma magnesium concentration or pH were detected after exercise. Plasma PTH concentration was not increased after exercise in 8 horses; in these horses, plasma PTH concentration decreased from 58.2 ± 26.3 to 27.4 ± 22.4 pg/ml, although plasma Ca2+ concentration was also decreased.
Conclusions and Clinical Relevance—Plasma Ca2+ concentration was decreased after racing for 80 km, compared with values obtained before racing. In most horses, an increase in plasma PTH concentration that was commensurate with the decrease in plasma Ca2+ was detected; however, some horses had decreased plasma PTH concentrations. (J Am Vet Med Assoc 2001;219:488–490)