The Reticulo-Endothelial System (R.E.S.) in Traumatic Shock

Abstract

Early in shock the Sympathetic Nervous System is hyperactive in response to deficient perfusion of tissues. This response maintains capillary hydrostatic pressure essential for exchanges between tissues and blood¹. Prolonged sympathetic overactivity further reduces tissue perfusion and causes functional damage of all organs particularly in the liver and spleen which are very sensitive to hypoxia. Since these organs contain the largest fraction of the defense against bacteria and bacterial endotoxin, it is in such circumstances that endotoxin of intestinal origin can reach the systemic circulation in its still toxic state². The resulting endotoxemia increases the ischemia of the tissues for endotoxin and catecholamines act sinergistically to damage the peripheral circulation³. Further decline of the peripheral flow causes generalized disorganization at the cellular level. The vascular smooth muscle cells develop structural changes⁴ and consequently there is a loss of vascular tone and hyporeactivity of the vessels to catecholamines. A disproportionate amount of blood is retained in the peripheral bed so that progressive decline in venous return to the heart occurs. Cardiac output falls progressively. Death results when there is not enough blood to sustain the minimal requiriments of vital organs.