Dexamethasone treatment during hemorrhagic shock: changes in extracellular fluid volume and cell membrane transport

Changes in extracellular fluid volume and cell membrane transport during hemorrhagic shock and the effects of dexamethasone treatment on these changes were measured. It is well known that prolonged hemorrhagic shock leads to irreversible changes and a progressive decrease in blood pressure despite reinfusion for lost blood. Pharmacologic doses of glucocorticoids provide some protection against these changes. Therefore, one purpose in the present study was to identify possible sites of glucocorticoid action whicy may prevent the irreversible changes from occurring. The extracellular fluid volume in normal control, nontreated dogs in shock, and dexamethasone-treated dogs in shock were measured by a dilution technique, using [35S] sodium sulfate. Cell membrane cation transport capabilities were measured in liver slices, diaphragm slices, and red blood cells taken from normal control, nontreated rats in shock, and dexamethasone-treated rats in shock. The accumulation of radioactivity by the tissues incubated with 22Na served as an indicator of cell membrane ion transport capabilities. The results indicate that in animals subjected to prolonged hemorrhagic shock, there is a fluid shift from the extracellular space into intracellular spaces, reducing blood volume. Cell membranes are damaged and transport mechanisms are altered; therefore, the cells are unable to extrude ions along with water. Dexamethasone treatment was shown to prevent extracellular fluid volumes from decreasing below that amount due to the plasma lost during hemorrhage. Also, it prevented some cell membrane damage and maintained membrane transport mechanisms near normal. In addition, at the onset of dexamethasone injection, blood pressure increased, and urine output was restored.