Mechanisms involved in the adrenaline-induced blockade of milk ejection in dairy cattle.

To elucidate mechanisms by which epinephrine (epi) blocks milk ejection in cattle, blood serum oxytocin (OT) concentrations were measured in four heifers before, during, and after milking following either intrajugular injection of 0.85% saline (S) or epi (3 mg). S did not affect OT concentrations. They peaked 2 min after milking-machine attachment. OT declined 3 min after milking commenced, reaching resting concentrations 10-60 min after milking. Milk yields were not altered by S. Epi did not influence significantly basal OT concentration. Yet, OT released to milking appeared less than the saline control. Peak OT concentration after epi and milking was reached 1 min after machine attachment. OT declined within 3 min after milking commenced. Milk yield was reduced 48% after epi. Jugular vein and carotid arterial OT concentrations and mammary blood flow (MBF) were measured simultaneously in four multiparous cows. Blood was collected before, during, and after milking following S or epi (50 micrograms). Jugular and carotid OT concentrations followed similar patterns for both treatments. Changes in carotid OT concentrations lagged behind those of the jugular vein by approximately 1 min. Elevated carotid OT concentrations were seen in two cows after milking and thought to be derived from non-hypothalamic-neurohypophysial sources. Epi (50 micrograms) did not reduce blood OT concentrations, but reduced MBF by 95%. Milking induced increases in MBF seen in controls, were not observed with epi, and milk yield was reduced by 56%. Our experiments suggest that epi may inhibit OT release to milking stimuli at pharmacological doses. At lower doses, epi exerts its effects peripherally by acutely reducing MFB, thus preventing physiological concentrations of hormone from reaching the myoepithelium. An intrinsic action of epi on the myoepithelial cells of cattle is unlikely, but cannot be ruled out at this time.