Abstract

Mammary arterious − venous differences (A − V) and excretion into milk of four prostanoids were related to changes in milk yield and milk vein blood velocity (MBV) in goats at different stages of pregnancy and lactation, and during somatotropin (ST) treatment in mid-lactation. Arterial concentrations and mammary A − V for the vasodilators prostacyclin (PGI 2) and prostaglandin (PG) E 2 (measured as 6-keto-PGF 1α and bicyclic PGE 2, respectively) decreased from late pregnancy to lactation. A − V were negatively correlated to MBV ( r = −0.32 to −0.34). Arterial concentrations of the vasoconstrictors PGF 2α and TXA 2 (measured as TXB 2) changed similarly, but no A − V across the mammary gland were found. The vasodilator to vasoconstrictor ratio in plasma was around 1:1, and in skimmed milk around 0.29–0.49 due to significantly higher TXB 2 levels in milk compared to plasma. Close linear correlations were established between milk yield and excretion of TXB 2 into milk ( r = 0.80, P < 0.001), and between MBV and PGE 2 excretion into milk ( r = 0.69, P < 0.001). ST treatment stimulated MBV and mammary prostanoid supply, and decreased prostanoid concentration in milk vein plasma. The high arterial levels of prostaglandins during pregnancy most likely reflected uterine synthesis. Our results support a role for PGI 2 and PGE 2 in local mammary blood flow regulation during lactation. Increased mammary uptake of these two prostanoids may be involved in the mammary blood flow response to ST. TXA 2 may be synthesized by mammary epithelial as well as vascular cells, and TXA 2 may be an important factor in regulation of mammary function.

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