PROTECTION AGAINST ACUTE TRAUMA AND TRAUMATIC SHOCK BY VASODILATORS

Abstract

The effects of hydralazine and Dibenzyline, agents which induce vasodilatation by different mechanisms, on the development of shock were studied in rats subjected to two levels of trauma in a Noble–Collip drum. Hydralazine effectively reduced the incidence of acute traumatic deaths (those occurring during or within 15 minutes after completion of the period of trauma), but it protected against late, shock deaths and improved over-all survival only among animals subjected to relatively mild trauma. Dibenzyline completely eliminated all late, shock deaths and increased over-all survival at both levels of trauma. The total incidence of early deaths was unaltered, but among Dibenzyline-treated animals a higher percentage of these occurred during the period of trauma, indicating some increased susceptibility to the immediate effects of acute trauma. The drug also caused some increase in the incidence of intraperitoneal hemorrhage due to rupture of the liver or spleen. Vascular engorgement of these organs, which increased during the drumming period in both control and Dibenzyline-treated animals, was not altered by the drug. The results of combined administration of hydralazine or polyvinylpyrrolidone (PVP) and Dibenzyline were qualitatively and quantitatively the same as those obtained with Dibenzyline alone. These data indicate that vasodilatation induced by inhibition of sympathetic vasoconstriction provides effective protection against death from shock, but may increase susceptibility to the immediate deleterious effects of acute trauma. A drug such as hydralazine, which can increase cardiac output, and acute expansion of plasma volume by PVP may sustain the circulation, particularly the cerebral circulation, during acute trauma, but do not effectively increase ultimate survival.