BACKGROUND: Loss of calcium around calving can lead to diseases of transition period and reduce animal economic life. Prevention of milk fever and subclinical hypocalcemia is crucial and important in this period. Repeated doses of oral calcium chloride at calving is a method to prevent hypocalcemia and associated complications. ObjectiveS: The objective of this study was to evaluate the influence of oral calcium chloride at calving on serum calcium, phosphorus and magnesium in transitional period of Holstein dairy cows fed with anionic and cationic diets. Methods: Forty-two Holstein dairy cows were randomly divided in 3 groups. Group 1 (n = 14), fed diet with negative DCAD without calcium chloride supplementation. Group 2 (n = 14), fed diet with negative DCAD and supplemented with calcium chloride at calving and 12 h later. Group 3 (n = 14), fed diets with positive DCAD and supplemented with calcium chloride at calving and 12 h later. Blood samples were collected at calving and 6 h and 12 h and 1d, 2 d, 7 d, 14 d, 21 and 28 d after calving. Serum concentrations of Ca, P and Mg were measured by conventional methods. Results: The pattern of changes in serum levels of calcium and magnesium in different groups in different time periods (time × treatment interaction) were different (p<0.0001). Changes in serum phosphorus levels in different time periods were statistically significant (p<0.0001), but its mean was not affected by the treatment groups (p=0.7164).                    ConclusionS: In addition to anionic diets, supplemental calcium chloride should be used to prevent subclinical hypocalcemia in high-producing dairy cows.

Changes in immune factors expressed by milk somatic cells from Holstein cows with hypocalcemia after calving were investigated in this study. Fourteen multiparous Holstein cows after their 3rd or 4th calving in one farm were used. The cows were divided into 2 groups: 7 cows needing treatment due to onset of hypocalcemia (hypocalcemia group; age = 5.53 ± 0.27 years, parity = 3.14 ± 0.14) and 7 cows without health problems (control group; age = 5.88 ± 0.31 years, parity = 3.57 ± 0.26). Milk samples were collected aseptically using a cannula and mRNA of immune factors expressed by milk somatic cells were analyzed. Milk samples (50 mL) were collected from the right rear mammary gland of cows before milking at day 1 and weeks 1, 2, 4, and 8 after calving. All milk samples showed a negative reaction to the California Mastitis Test. Levels of relative interleukin (IL)-6 and cathelicidin in the hypocalcemia group were lower than those in the control group in weeks 1 to 8. A significant difference in relative IL-6 levels was found in week 4 (P < 0.05). These results suggest that levels of IL-6 expressed by milk somatic cells may be affected by hypocalcemia in dairy cows.

Feline serum samples (n = 434) were classified as hypercalcemic, normocalcemic, or hypocalcemic based on both total calcium (tCa) and ionized calcium (iCa) concentrations. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), positive diagnostic likelihood ratio (PDLR), and negative diagnostic likelihood ratio (NDLR) were calculated for prediction of hypercalcemia and hypocalcemia in all samples, in hypoalbuminemic cats, and in those with chronic renal failure (CRF) as compared with cats that had other conditions. Diagnostic discordance in prediction of iCa using tCa was 40%. Sensitivity of tCa in prediction of ionized hypercalcemia was low and specificity was high. The PDLR for prediction of ionized hypercalcemia or hypocalcemia was low in all cats, especially in those with CRF. Due to the high level of diagnostic discordance, tCa should not be used to predict iCa concentration. Concentration of iCa should be measured directly when accurate assessment of calcium status is needed.

Objective-To evaluate the effects of metabolic acidosis and changes in ionized calcium (Ca(2+)) 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, Ca(2+) 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.