HIGH CORTISOL CONCENTRATIONS AND MEDIATION OF THE HYPOGALACTIA DURING ENDOTOXIN-INDUCED MASTITIS

A series of experiments was conducted to define the role of cortisol in the hypogalactia during endotoxin-induced mastitis. In the first experiment, three of six nonmastitic cows were given a continuous infusion of trilostane, a 3-beta-hydroxysteroid dehydrogenase inhibitor that blocks enhanced cortisol synthesis. Trilostane had no effect in these cows. In the second experiment, six midlactation cows were given 10-mu-g of endotoxin in each of two homolateral quarters to induce mastitis. Three of these cows also received trilostane. Increased serum cortisol following endotoxin infusion was blocked by trilostane treatment, whereas serum glucose and rectal temperatures were unaffected. Preventing the cortisol increase failed to reduce hypogalactia in endotoxin-infused or uninfused quarters. Decreases in milk production and increases in measures of mammary inflammation were greater in trilostane-treated cows, indicating that endogenous cortisol may moderate the cow's inflammatory response. In the third experiment, three of six nonmastitic cows were injected intramuscularly with 150 IU of ACTH. Serum cortisol concentration exceeded 70 ng/ml for at least 3 h in cows receiving ACTH. This cortisol concentration, comparable with concentrations found during endotoxin mastitis, did not inhibit milk production. Together, these data demonstrate that the acute cortisol increase does not mediate the hypogalactia associated with endotoxin-induced mastitis.