Pathophysiology of circulatory shock: an overview

Recent developments in three categories of shock research are discussed. Organ perfusion and humoral pathophysiological responses were investigated first, since the cause of fatal shock is always ischemia, tissue hypoxia and resulting cell damage with abolishment of mitochrondrial function. Both centrally and peripherally administered thyrotropin-releasing hormone (TRH) had vasopressor effects that are mediated by a central cholinergic mechanism. A derivative of TRH, DN-1417, had a longer-acting vasopressor action. TRH content increased in the brain in reversible shock, while amino acids increased in irreversible shock.