Disturbed Milk Ejection at Machine Milking and the Issues Related to Exogenous Oxytocin in Dairy Cows

Disturbed milk ejection (DME) can occur under various conditions in practical dairy farms. As a consequence udder emptying at milking is incomplete. If milk ejection is completely lacking, only the cisternal milk fraction is available, i.e., only 0–20% of the milk stored in the udder. The disturbance is due to an insufficient release of oxytocin in response to tactile udder stimulation. In all known situations in practical dairy farming, exogenous oxytocin even at a low dosage is suitable to overcome the disturbance. However, due to the short half-life of oxytocin this treatment is only effective for a short time, i.e., for one milking event. A sustainable therapy to activate endogenous oxytocin release in response to teat stimulation is currently not yet available. In some cases, albeit not always, vaginal instead of teat stimulation leads to a sufficient oxytocin release to induce milk ejection. DME can occur in primiparous cows during the first weeks postpartum, in unfamiliar surroundings (e.g., after the changeover to a new milking system) or during peak estrus. Also in housing systems where dairy cows are kept in contact with their calves DME at machine milking has been observed in some farms. Except for clinical mastitis or inadequate milking machine settings causing pain to the cow disturbed milk ejection can mostly not be linked to obviously observed stress. Also, typical stress-related hormones such as adrenaline have not been elevated at disturbed milk ejection, and exogenous cortisol or catecholamines do not inhibit the release of oxytocin during milking. Endogenous opioids may be involved in the disturbance as beta-endorphin has been elevated in some studies during DME, and exogenous morphine caused an inhibition of oxytocin release during machine milking. DME is mostly treated by oxytocin injection at each milking. However, all commercially available oxytocin preparations can be used only at a massive overdose causing circulating blood concentrations far beyond the physiological range. Whereas endogenously released oxytocin decreases immediately to baseline after milking, the injected oxytocin remains often elevated for several hours after injection. The consequence is the development of a reduced sensitivity of the mammary gland to oxytocin within a few days of repeated treatments. Even if the oxytocin release from the pituitary is normal, the high dosage oxytocin treatment cannot be stopped before the next dry off. Therefore, exogenous oxytocin treatment needs to be recommended at a dosage as low as possible and for the shortest possible period. The i.v. injection of 0.5–1 i.u. of oxytocin instead of the often used 20–50 i.u. is sufficient to empty the udder at machine milking. This is only possible if the oxytocin product is diluted in physiological saline to achieve a volume which can be injected from a practical point of view, i.e., to inject several ml instead of μl. Besides the reduced milk harvest with a direct impact on the farm income, periods of low or no milk flow during milking cause an increased mechanical load on the teat tissue through high vacuum both at the teat end and at the mouthpiece chamber of the liner. This in turn increases the risk of hyperkeratosis and increased teat tip callosity, and hence susceptibility to mastitis. Studies to detect a genetic background of the likelihood of disturbed milk ejection were without unambiguous results until today. It remains unclear why only some individual animals show disturbed milk ejection.