Abstract

Low concentrations of the essential amino acid histidine in circulation have been shown to increase mammary blood flow and it has been suggested that this effect is mediated by histamine. The hypotheses tested in this experiment were that interstitial histamine concentrations in the mammary gland are related to arterial His concentrations and that mammary blood flow is reduced by extracellular histamine via H1 receptors. The hypotheses were tested by infusing saline or chlorpheniramine, a blocker of the H1 histamine receptor, into the arterial supply of the mammary glands of lactating cows infused with 44 gh of amino acid mixtures with or without His for 10h. Infusates were administered in a 2×2 factorial arrangement within a 4×4 Latin square to 4 multiparous Holstein cows in mid lactation. Exclusion of His from the infusate decreased protein content in milk from the infused udder half from 3.98 to 3.77%, and increased arterial α;-aminonitrogen concentration from 3.2 to 3.4mM. Neither the decreased arterial His concentration nor the H1 blocker affected plasma flow to the infused udder half. We conclude that histamine is not involved in the regulation of mammary blood flow. The H1 blocker decreased milk production in the infused udder half from 4.6 to 3.5kg without affecting protein, fat, and lactose percentages, suggesting an inhibition of milk ejection. Cows on chlorpheniramine ate less feed during the infusion than saline-infused cows, which resulted in lower arterial concentrations and mammary uptakes of acetate. The efficiency of plasma triacylglycerol uptake across the mammary glands was decreased by chlorpheniramine but net uptake of long-chain fatty acids was not affected. The mechanism by which an amino acid deficiency influences mammary blood flow does not involve histamine signaling through the H1 receptor and remains unidentified.

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