PSIV-2 Changes in free glutamine and glutamate in mare milk during early lactation

Glutamine plays an important role in neonatal health. This amino acid serves as a nitrogen and amine carrier between tissues, as a major energy source and as a precursor for nucleic acids and proteins in rapidly proliferating intestinal cells. This study aimed to evaluate changes over time in free Gln and Glu concentrations in mare milk in early lactation and their relationship with foal gut health. Thirteen Thoroughbred mare and foal pairs were studied. Milk samples were collected at 12 h, 3, 5, 7, 10, 14, and 21 d after parturition and daily milk yield was estimated at 7 and 14 d postpartum. Milk samples were centrifuged (10 min, 3500 x g, 4 °C) to remove fat, then centrifuged twice (5 min, 10,000 x g, 22 °C) to remove protein. Free Glu and Gln were analyzed in triplicate using a membrane-based glutaminase and glutamate oxidase method (YSI 2700 Analyzer, YSI Life Sciences, OH). Daily fecal scores were recorded to monitor foal diarrhea and body weights were recorded weekly. Mixed model ANOVA with repeated measures (SAS 9.4) were used to evaluate changes over time in free Gln and Glu. Relationships between variables were assessed using regression analyses and Pearson’s correlation coefficient. Free Gln and Glu changed over time (P < 0.0001). Glutamine increased from 12 h to 5 d, (0.24±0.11 mmol/L and 1.09±.11 mmol/L, respectively; P < 0.05) then decreased to 0.90±0.11 mmol/L by 21 d postpartum. In contrast, free Gln was the lowest at 12 h (0.36±0.04 mmol/L) and continued increasing through 21 d postpartum (0.80±0.04 mmol/L; P < 0.05). Bouts of diarrhea were negatively related to milk Gln (P < 0.05) and foal ADG was positively related to milk Glu (P < 0.05). These results suggest that Gln may have a role in foal gut health while Glu may influence foal growth.

Synthesis and supramolecular assembly of fluorinated biogenic amine recognition host polymers

Fluorine functionalized biogenic amine carrier polymers.

Release of tritiated noradrenaline from perfused rat hearts by sympathomimetic amines

The hypothesis that the limiting factor controlling the noradrenaline-releasing activity of a sympathomimetic amine is the ability of the nerve ending to take up the amine, i.e. the affinity of the amine for the postulated amine carrier in the sympathetic nerve ending, was tested on perfused rat hearts labelled with tritiated noradrenaline (NA). Experiments were done to determine whether cocaine and desmethylimipramine (DMI) would block the releasing action of sympathomimetic amines (SMA) and to determine whether the ranking order of the releasing activity of a series of SMA corresponds to the order of affinity for the amine carrier as reported by Iversen. The releasing activity of NA was found to be a saturable process, reaching a maximum rate estimated to be 2.6% of the amount present in the heart per minute. In addition, cocaine and DMI competitively blocked the releasing activity of infused NA, adrenaline, and dopamine, but this inhibition could be overcome by increasing the dose of the SMA. The ranking order of releasing activity of this series of amines was l-noradrenaline, dopamine, l-adrenaline, p-tyramine, d-noradrenaline, d-adrenaline, l-isoproterenol, phenylethylamine, d-isoproterenol, which was approximately the same as their order of affinity for the amine carrier. Our results indicate that uptake by a membrane carrier is probably the limiting factor in the releasing activity of SMA which are catechols and have a β-OH group. However, those amines studied which do not have these structural properties, i.e. dopamine, tyramine, and phenylethylamine, are further limited in their releasing activity, possibly owing to a less rapid exchange at the binding site on the storage granule.