| The glucocorticoids inhibit the release of inflammatory mediators from macrophages and eosinophils but do not inhibit the release of granules from mast cells. Glucocorticoids decrease synthesis of prostaglandins, leukotrienes, and platelet-activating factor, which play important roles in the pathophysiology of respiratory tract diseases. Studies suggest glucocorticoids enhance the action of adrenergic agonists on β2 receptors in the bronchial smooth muscle.
Because of immunosuppressive effects, glucocorticoids are generally avoided in infectious respiratory diseases. |
| For severe attacks of allergic bronchitis, asthma, or RAI, parenteral injection of glucocorticoids usually provides rapid relief. For chronic therapy in small animals, oral prednisone is usually the drug of choice. Prednisone is a prodrug, as it is hepatically metabolized to the active drug prednisolone. Only animals with severe hepatic impairment and horses are unable to metabolize prednisone to prednisolone. A typical anti-inflammatory dosage is 0.5-1.0 mg/kg, with chronic
therapy on an every-other-day basis. Cats are somewhat resistant to the effects of glucocorticoids, and dosages of prednisone of 1.0 mg/kg/day may be necessary for chronic therapy of feline asthma. Alternatively, 20 mg of methylprednisolone acetate can be administered IM to asthmatic cats every 3 wk. For emergency treatment of dyspneic cats, a shock dose of an IV glucocorticoid (prednisone sodium succinate, 5-10 mg/kg; or dexamethasone sodium phosphate, 1-2 mg/kg) should be used.
Prednisone has a low oral bioavailability in horses. After administration of prednisone, only negligible plasma concentrations of prednisone or prednisolone are measured. While prednisolone can be administered to horses, the small tablet sizes available make it inconvenient, so equine formulations of oral dexamethasone are recommended. The injectable formulation of dexamethasone can be given IV to horses with acute bronchoconstriction and dyspnea. |
