Interaction of 5-hydroxy-l-tryptophan and negative dietary cation-anion difference on calcium homeostasis in multiparous peripartum dairy cows.

Hypocalcemia affects almost 50% of all dairy cows. Our laboratory has previously demonstrated that infusions of the serotonin precursor 5-hydroxy-l-tryptophan (5-HTP) increase circulating calcium concentrations in the Holstein transition cow. It is unknown whether feeding a negative dietary cation-anion difference (DCAD) diet alters the relationship between 5-HTP and hypocalcemia. The main objective of this study was to determine whether feeding a negative DCAD (-DCAD) diet before calving in conjunction with 5-HTP treatment could further diminish the magnitude of hypocalcemia at the time of calving. We used a randomized complete block design with a 2 × 2 factorial arrangement. Thirty-one multiparous Holstein cows were fed either a positive (+13 mEq/100 g) or negative (-13 mEq/100 g) DCAD diet 21 d before parturition and were intravenously infused daily with saline or 5-HTP (1 mg/kg) starting 7 d before the estimated date of parturition. Cows were blocked by parity and were randomly assigned to 1 of 4 treatment groups: positive DCAD plus saline, positive DCAD plus 5-HTP, negative DCAD plus saline, and negative DCAD plus 5-HTP, resulting in n = 8 per group. Total calcium (tCa), ionized calcium (iCa), and feed intake were recorded. The iCa was elevated prepartum in the -DCAD/5-HTP group compared with the other treatment groups as well as on d 0 and 1 postpartum. Although differences in tCa were not significant across the pre- or postpartum periods, tCa was numerically higher on d 0 and significantly higher on d 1 in -DCAD/5-HTP cows compared with all other groups. Prepartum the -DCAD/5-HTP treatment group ate less than the other treatment groups; however, postpartum dry matter intake differences were not significant. These findings demonstrate that feeding a -DCAD diet in conjunction with 5-HTP prepartum can increase postpartum circulating iCa concentrations and therefore diminish the magnitude of hypocalcemia at the time of parturition.

Effect of incomplete milking on milk production rate and composition with 2 daily milkings.

The primary aim of this study was to assess the effects of incomplete milking on milk secretion and milk composition at the quarter level. Twelve cows were enrolled beginning at 5 d in milk and remained on study through 47 d in milk. Half of each contralateral udder was incompletely milked (treatment), detaching the teat cup early to leave approximately 30% of the total milk yield behind. This target milk remaining in the gland was based on weekly calibration milking measurements of quarter total milk yield. Control quarters were milked completely until milk flow had decreased to 0 kg/min based on visual assessment. Harvested milk yield was measured twice daily at each milking, and milk components (fat, protein, lactose, solids nonfat, milk urea nitrogen) and somatic cell count, were measured twice weekly at the quarter level. The experimental unit in this design was the half-udder, and a mixed-model approach was used to assess the main and interactive effects of experiment week and treatment on milk production rate, milk remaining in the gland, and milk composition. The effect of treatment on milk production rate was significant, with the average control half-udder producing 0.97 kg/h and the treatment half-udder 0.73 kg/h. The effect of week on milk production rate and the interaction of week × treatment were also significant. The effect of treatment on milk remaining in the gland was significant, illustrating that an increase in milk remaining in the cisternal compartment had been achieved. We detected a significant decrease in milk lactose percentage in treatment half-udders, and a significant increase in somatic cell count (log10). The increase was relatively small, from a geometric mean of 26,300 cells/mL in control quarters to 48,300 cells/mL in treatment quarters. The decrease in milk production rate in treatment half-udders supports current knowledge about how mammary epithelial cell secretion, proliferation, and apoptosis are modulated by autocrine-paracrine factors.