There is evidence for a physiological role of the adrenal cortex in the early responses to limb ischemia in the rat. Trilostane, which inhibits steroid production and prevents the usual rise in corticosterone concentration, impairs compensatory fluid movement during the 3 h after removal of bilateral hindlimb tourniquets and truncates the accompanying hyperglycemia. We have now studied whether altering the corticosterone concentration has similar effects over a 3-h period after a 35% hemorrhage in the conscious rat. After hemorrhage there was only a small rise in plasma glucose concentration, which was unaffected by inhibition of the adrenocortical response with trilostane or its prolongation with adrenocorticotrophic hormone. However, if hindlimb tourniquets were applied 4 h beforehand, the hyperglycemia after hemorrhage was as large as after tourniquet removal and was similarly curtailed by trilostane. Compensatory fluid movement, in contrast, was unaffected by any of the alterations in corticosterone concentration, with or without tourniquets. Thus the method of producing fluid loss is critical in determining whether glucocorticoids play a role in compensation but not in maintaining hyperglycemia after injury.
The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system?