Preservation of cellular integrity as a protective mechanism of dexamethasone in hemorrhagic shock in the cat.

Anesthetized cats were hemorrhaged to a mean arterial blood pressure of 40 mm Hg for 120 minutes. Cats given dexamethasone (6 mg/kg, i.v.) at the time of hemorrhage and again (3 mg/kg, i.v.) at the time of reinfusion maintained post-reinfusion arterial blood pressure at a higher level than cats given the steroid vehicle. In addition, dexamethasone treated cats exhibited higher post-reinfusion liver blood flows than vehicle treated hemorrhaged cats. Dexamethasone significantly retarded the rise in plasma cathepsin D and amino-nitrogen activities during hemorrhage, and prevented the accumulation of a myocardial depressant factor (MDF) in the circulating blood. Dexamethasone had no significant effect on isolated cat papillary muscle or aortic strips. It appears that dexamethasone exerts its beneficial effect in hemorrhage shock primarily by stabilizing lysosomal membranes and the subsequent prevention of proteolysis and MDF formation rather than by a direct vasodilator or inotropic effect.